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MK ACVD Exam > Pharmacology (not done) > Flashcards

Pharmacology (not done) Flashcards

1
Q

What is the MOA of lidocaine/pramoxine?

A

Sodium channel antagonist –> interferes with impulse production and action potential in nerves

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2
Q

What is the MOA of capsaicin?

A

TRPV1 agonist on C nerve fibers –> depolarization and neural desensitization

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3
Q

What is the MOA of topical menthol?

A

TRPM8 antagonist –> cooling sensation (no major benefits in dogs to date)

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4
Q

What is the MOA of antihistamines?

A

H1 receptor antagonists –> competitively block formation of histamine-receptor complex

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5
Q

What is the MOA of maropitant for itch?

A

Neurokinin-1 receptor inhibitor

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6
Q

What is the MOA of lokivetmab?

A

Anti-canine IL-31 mAB –> binds to circulating IL-31 and prevents it binding to its receptor

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7
Q

What is the MOA of ranevetmab?

A

Anti-canine nerve growth factor mAB (fails to prevent atopic itch)

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8
Q

What is the MOA of gabapentin and pregabalin?

A

GABA analog (inhibitory neurotransmitter) –> inhibits voltage-gated Ca channels in spinal cord –> reduces central neural hypersensitization

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9
Q

What is the MOA of topiramate?

A

NMDA receptor antagonist –> increases GABA activity and inhibits glutamate activity –> less neuronal excitability

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10
Q

What is the antipruritic MOA of butorphanol?

A

Mixed kappa-opioid agonist and mu-opioid antagonist

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11
Q

Would naloxone be potentially antipruritic?

A

Yes because it is a mu-opioid antagonist

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12
Q

What is the antipruritic MOA of amantadine?

A

NMDA receptor antagonist –> less neuronal excitability

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13
Q

What is the MOA of amitriptyline?

A

Tricyclic SSRI –> inhibits reuptake of serotonin –> increased neural impulses

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14
Q

What is the MOA of clomipramine?

A

Tricyclic SSRI –> inhibits reuptake of serotonin
(potent SSRI but not very specific)

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15
Q

What is the MOA of fluoxetine?

A

Bicyclic SSRI–> inhibits reuptake of serotonin
(very selective)

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16
Q

What is the MOA of doxepin?

A

SNRI –> inhibits reuptake of serotonin and norepi –> increased neurotransmission
Also has potent anti-H1 receptor properties

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17
Q

What is the MOA of mirtazapine?

A

SNRI –> antagonizes serotonergic and noradrenergic receptors
(useful for nocturnal pruritus)

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18
Q

How does vitamin E help in treatment of SNP?

A

Reduces damage from lipid peroxidation

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19
Q

What drug has been associated with a drug-induced panniculitis?

A

KBr

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20
Q

What is the MOA of itraconazole?

A

inhibits 14alpha demethylase –> prevents conversion of lanosterol to ergosterol

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21
Q

At which pH is oral itraconazole best absorbed?

A

Acidic (so giving with food helps)

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22
Q

What cutaneous adverse effect has been associated with itraconazole in dogs?

A

Vasculitis/ulcers (>10 mg/kg dose)

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23
Q

What is the MOA of ketoconazole?

A

Inhibits lanosterol 14alpha demethylase –> ergosterol depletion, accumulation of toxic sterols in the cell membrane

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24
Q

Which antifungal interferes with endogenous steroid synthesis?

A

Ketoconazole

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25
Q

What azole does not require food for optimal absorption?

A

Fluconazole

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26
Q

Which oral antifungal medication has the highest MIC (and thus the least efficacy) against dermatophytes?

A

Fluconazole

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27
Q

What is the MOA of terbinafine?

A

reversibly inhibits squalene epoxidase –> prevents conversion of lanosterol to cholesterol/ergosterol

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28
Q

Does terbinafine affect cytochrome P450?

A

No

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29
Q

What oral antifungal has the lowest MIC against Microsporum sp. and Trichophyton spp?

A

Terbinafine

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30
Q

What is the MOA of griseofulvin?

A

Arrests metaphase –> inhibition of nucleic acid synthesis and cell mitosis
Interferes with spindle microtubules

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31
Q

What is a potential side effect of griseofulvin in cats?

A

Bone marrow suppression (idiosyncratic)

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32
Q

What is the MOA of lufenuron for dermatophytosis?

A

disrupts chitin synthesis (this drug is NOT recommended for tx)

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33
Q

What are the primary side effects of meglumine antimoniate?

A

Cellulitis/abscesses at injection site
Nephrotoxicity

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34
Q

What is the MOA of allopurinol for tx of Leishmania?

A

Hypothanine compound –> metabolized by Leishmania and produces an inosine analogue –> analogue incorporated into Leishmania RNA –> faulty protein translation and inhibition of multiplication

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35
Q

How should allopurinol be administered?

A

Orally with a low purine diet

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36
Q

How does marbofloxacin help with treatment of Leishmania?

A

Increases production of NO by macs –> increased kill
Stimulates TNF-a production

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37
Q

When should TT4 be assessed for a patient on once-daily dosing of thyroid supplement?

A

Pre-pill/at time med is due (>1.5 mcg/dL is adequate)

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38
Q

What medication is FDA-approved for treatment of Cushing’s disease?

A

Trilostane

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39
Q

You have a dog on unequal doses of trilostane BID. After which dose should an ACTH stim be done for dose monitoring?

A

3-5 hr after the higher dose is given

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40
Q

How long should glucocorticoids be withdrawn prior to an ACTH stim or LDDST?

A

Oral/otic/opthalmic short-acting: 2 weeks
long acting: 4 weeks

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41
Q

At what time of day should a blood sample be collected when monitoring a hyperthyroid cat on methimazole?

A

Any time of day (does not matter when the med was given)

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42
Q

What is the effect of food on absorption of levothyroxine?

A

Reduces absorption (best given on empty stomach)

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43
Q

What is the MOA of methimazole?

A

Inhibits thyroid peroxidase

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44
Q

What are the main SE of lomustine?

A

Myelotoxicity

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45
Q

What is the MOA of doxorubicin?

A

Antitumor antibiotic that inhibits topoisomerase II

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46
Q

What is the MOA of imiquimod?

A

Activation of TLR7 –> secretion of IFN-a, TNF-a, IL-6
Activation of Langerhans cells
Activation of macs, NK cells, B-cells

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47
Q

What type of cells are targeted by palmitoylethanolamide (PEA)?

A

Mast cells

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48
Q

What is the MOA of PEA?

A

Mast cell stabilizer

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49
Q

What causes PEA to be released by the body?

A

Stress and tissue damage

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50
Q

True or false: skin levels of PEA are higher in healthy dogs compared to atopic dogs

A

False - they are 30-fold higher in atopic dogs

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51
Q

What is the active ingredient in Redonyl Ultra?

A

Ultra-micronized palmitoylethanolamide (PEA)

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52
Q

Are glucocorticoids lipophilic or non-lipophilic?

A

Lipophilic

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53
Q

Where are glucocorticoid receptors located?

A

In the cell cytoplasm

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54
Q

What occurs after a glucocorticoid binds to its receptor in the cytoplasm?

A

It translocates into the nucleus via importins

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55
Q

What does a ligand-bound glucocorticoid receptor bind to within the cell nucleus to reduce inflammation?

A

Glucocorticoid response elements (+GREs)

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56
Q

What genes are produced once a +GRE is bound by a ligand-bound glucocorticoid receptor?

A

Annexin-A1 (ANAX1)/lipocortin 1
GC-induced leucine zipper (GLIZ)
Mitogen-activated protein kinase phosphatase 1 (MPK1)

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57
Q

Besides directly interacting with DNA, how else can glucocorticoid receptors affect gene transcription?

A

Tethering: interaction with transcription factors themselves

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58
Q

What family of proteins is synthesized when a ligand-bound glucocorticoid receptor binds to DNA?

A

IkBs

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59
Q

How to IkBs affect inflammation?

A

They inhibit NF-kB, a major transcription activator for inflammation

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60
Q

How do glucocorticoids affect NF-kB?

A

They increase the amount of IkBs, which inhibit NF-kB activity

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61
Q

What 2 DNA sequences can ligand-bound glucocorticoid receptors bind to?

A

+GREs
nGREs

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62
Q

How do glucocorticoids affect leukotriene synthesis?

A

They enhance lipocortin production –> inhibits PLA2 –> interrupts arachidonic acid metabolism –> less leukotriene synthesis

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63
Q

What type of T-cells are primarily inhibited by glucocorticoids?

A

Th1

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64
Q

What cytokines are reduced by glucocorticoids?

A

IL-1
IL-6
IL-8
IL-12
TNF-a
IFN-gamma
(Th1 cytokines)

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65
Q

What cytokines are upregulated by glucocorticoids?

A

IL-4
IL-10
IL-13

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66
Q

What transcription factor is upregulated by glucocorticoids and what cell type is subsequently upregulated?

A

FoxP3
Treg cells

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67
Q

In which species do glucocorticoids not have any effect on neutrophil phagocytosis?

A

Horses
Goats

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68
Q

How do glucocorticoids reduce acute inflammation?

A

Prevent vasodilation and prevent increased vascular permeability

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69
Q

Which glucocorticoids have less sodium retention activity?

A

Prednisone/prednisolone
methylprednisolone

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70
Q

Which glucocorticoid has a high degree of sodium retention activity?

A

Hydrocortisone

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71
Q

What enzyme converts prednisone to prednisolone and where does this occur?

A

11-beta-hydroxysteroid dehydrogenase type 1
Liver

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72
Q

A dog with hepatic disease requires glucocorticoids. You have a choice between prednisone and prednisolone - which should be chosen?

A

Prednisolone (liver is responsible for conversion of prednisone to prednisolone)

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73
Q

Why are cats less responsive to typical steroid doses?

A

They have fewer glucocorticoid receptors in the liver and skin and receptors have lower affinity

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74
Q

What medication is derived from the fungus Beauveria nivea/Tolypocladium inflatum?

A

Cyclosporine

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75
Q

What class of drugs is cyclosporine?

A

Calcineurin inhibitor

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76
Q

What transcription factor is dephosphorylated by calcineurin?

A

Nuclear factor of activated T-cells (NFAT)

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77
Q

What is the MOA of cyclosporine?

A

Binds to cyclophilin intracellularly (within T-cells) –> this complex binds to calcineurin and inhibits its dephosphorylating activity –> prevents translocation of NFAT into the cell nucleus –> suppressed cytokine production and impaired T-cell activation

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78
Q

What cytokines are upregulated by NFAT activity in the nucleus?

A

IL-2
IL-4
TNF-a
TNF-gamma

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79
Q

True or false: It is acceptable to use compounded cyclosporine formulations in dogs.

A

False

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80
Q

What enzyme metabolizes cyclosporine and where does this occur?

A

CYP3A family (CYP3A4, CYB3B5)
occurs in liver

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81
Q

What mutation in dogs would warrant you to be cautious of CsA dosing as typical dosing could cause excessive immunosuppression?

A

MDR1

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82
Q

Why is cyclosporine a potential concern in patients with an MDR1 mutation?

A

It is a substrate of the p-glycoprotein efflux pump–> can accumulate if pump is defective due to MDR1 mutation (reduced biliary excretion)

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83
Q

What would the expected response to typical CsA doses be in a dog with diabetes?

A

Less response to typical dose due to increased clearance/reduced half-life

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84
Q

How long is it “safe” to store Atopica capsules in the freezer at -20 degC?

A

1 month

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85
Q

What type of drug is azathioprine?

A

pro-drug of 6-mercaptopurine (6-MP)

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86
Q

Which metabolites of azathioprine have no immunosuppressive effect?

A

6-thiouric acid
6-merthymecaptopurine (6-MMP)

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87
Q

What metabolite of azathioprine has cytotoxic/immunosuppressive effects?

A

6-thioguanine nucleotide (6-TGN)

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88
Q

What are the 3 metabolites of azathioprine?

A

6-thioguanine nucleotide (immunosuppressant)
6-thiouric acid (not immunosuppressant)
6-merthymecaptopurine (not immunosuppressive)

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89
Q

In what parts of the body does azathioprine conversion to 6-mercaptopurine occur?

A

RBCs
Intestinal wall
Liver

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90
Q

Which enzymes result in conversion of 6-MP to inactive metabolites?

A

Xanthine oxidase
Thiopurine-S-methyltransferase (TMPT)

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91
Q

Which enzyme results in the conversion of 6-MP into a cytotoxic metabolite?

A

Hypoxanthine-guanine phosphoribosyl-transferase (HPRT)

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92
Q

Which enzyme converts 6-mercaptopurine into 6-merthymecaptopurine?

A

Thiopurine-S-methyltransferase (TPMT)

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93
Q

Which enzyme converts 6-mercaptopurine into 6-thiouric acid?

A

xanthine oxidase

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94
Q

What enzyme converts 6-mercaptopurine into 6-thioguanine nucleotide?

A

hypoxanthine-guanine phosphoribosyl-transferase (HPRT)

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95
Q

How does azathioprine affect DNA synthesis?

A

It’s active metabolite (6-TGN) acts as a false purine –> incorporated into DNA –> mutated DNA, cell cycle stops

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96
Q

What cells are most affected by azathioprine?

A

Actively dividing cells (T-cells, B-cells, thrombocytes)

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97
Q

How does azathioprine affect leukocyte adhesion to endothelium?

A

6-MP inhibits RAC1 which is important for formation of ICAM-1 and VCAM-1

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98
Q

How does azathioprine affect T-cell migration, adhesion, and proliferation?

A

Inhibits RAC1 and BCL-XL

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99
Q

Responses from which T-cell subset are primarily blocked by CsA?

A

CD4+ (T-helper)

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100
Q

How long after dosing does oral CsA reach peak blood levels?

A

2 hours

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101
Q

Why should allopurinol be avoided when using azathioprine?

A

It inhibits xanthine oxidase –> causes more production of the cytotoxic metabolite of AZA (6-TGN)

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102
Q

What drugs should be avoided when using allopurinol for treatment of Leishmaniasis?

A

Anticoagulants
Azathioprine
Cyclophosphamide
Diuretics
TMS
Urinary acidifiers

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103
Q

Why should azathioprine be avoided in cats?

A

They are deficient in thiopurine-S-methyltransferase and therefore make less of the inactive metabolite and more of the cytotoxic metabolite –> increased risk of myelosuppression

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104
Q

What breed of dog is more susceptible to azathioprine toxicity and why?

A

Giant Schnauzers
They have less active thiopurine-S-methyltransferase activity, leading to more production of cytotoxic metabolites

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105
Q

What breed of dog may require higher doses of azathioprine and why?

A

Alaskan Malamutes
They have higher thiopurine-S-methyltransferase activity and therefore make more inactive metabolites

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106
Q

Combining azathioprine with which other immunosuppressant can cause an increased risk of pancreatitis?

A

Glucocorticoids

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107
Q

What are 3 primary side effects of azathioprine?

A

GI upset
Myelosuppression
Hepatotoxicity

108
Q

What is the median time to onset of AZA-induced hepatotoxicity?

A

14 days (so check within 2 weeks of starting)

109
Q

What type of drug is chlorambucil?

A

Alkylating agent (nitrogen mustard group)

110
Q

What is the active metabolite of chlorambucil and where does this conversion occur?

A

Phenylacetic acid
Occurs in liver

111
Q

How long could it take to see the therapeutic effects of chlorambucil?

A

2 weeks

112
Q

What is the MOA of chlorambucil?

A

Converted into phenylacetic acid–> causes cross-linking of DNA at the guanine-N7 position –> DNA mutation and cell death

113
Q

What type of cells is chlorambucil most effective on?

A

Lymphoid cells (esp B-cells)

114
Q

What are the potential adverse effects of chlorambucil?

A

GI
Myelosuppression
Myoclonus
Fanconi syndrome

115
Q

What is the brand name of chlorambucil?

A

Leukeran

116
Q

What is the active metabolite of mycophenolate mofetil?

A

Mycophenolic acid (MPA)

117
Q

What is the MOA of mycophenolate?

A

Converted to active metabolite MPA –> inhibits inosine monophosphate dehydrogenase enzyme (IMPDH) in the de novo pathway –> inhibition of guanine nucleotide synthesis –> less DNA production –> fewer lymphocytes

118
Q

How is mycophenolate eliminated from the body in humans and dogs?

A

Glucuronidation

119
Q

What is the suspected elimination route of mycophenolate in cats?

A

Glucosidation (and therefore the lack of glucuronyl transferase enzyme is unlikely to be of major concern because glucuronidation does not occur in this species)

120
Q

What are the primary side effects of mycophenolate?

A

GI upset

121
Q

Which JAK is preferentially inhibited by oclacitinib?

A

JAK1

122
Q

What are the 4 JAK family members?

A

JAK1
JAK2
JAK3
TYK2

123
Q

What occurs once a cytokine binds to a cytokine receptor attached to JAKs?

A

The JAKs are phosphorylated –> STATs bind and are phosphorylated –> STATs released into cytoplasm and bind other STATs –> STATs translocate into nucleus and bind to DNA for gene transcription

124
Q

What JAKs are associated with the binding of cytokines involved in hematopoiesis and innate immunity?

A

JAK2/JAK2
JAK2/TYK2

125
Q

What cytokines have been shown to be reduced when using high extra-label doses of Apoquel?

A

IL-2
IL-15
IL-18
IFN-gamma
(inhibition of T-cell proliferation)

126
Q

What are potential adverse effects of high doses of Apoquel in dogs?

A

Impaired T-cell proliferation –> increased infection risk

127
Q

What JAKs are typically used by IFN-gamma receptors?

A

JAK1
JAK2

128
Q

What JAKs are used by IL-4 receptors?

A

JAK1
JAK3

129
Q

How does oclacitinib suppress Th2 responses?

A

Inhibits production of IL-2, IL-4, IL-6, IL-13

130
Q

How does oclacitinib block itch signaling?

A

Inhibits production of IL-31 and TSLP

131
Q

What is the primary cell type affected by Bruton’s tyrosine kinase inhibitors?

A

B-cells

132
Q

Which topical steroid has been demonstrated to have minimal effect on adrenocortical function?

A

Mometasone furoate

133
Q

What does tacrolimus bind to in order to suppress the NFAT pathway?

A

FK506 binding protein (aka FKBP12)

134
Q

What is the definition of AZA-induced hepatotoxicity?

A

ALT >2-fold the upper limit of the ref range

135
Q

What metabolite is responsible for the cytopenias seen with AZA?

A

6-TGN

136
Q

What would be expected in a dog with a thiopurine methyltransferase enzyme deficiency if given AZA?

A

Elevated thioguanine nucleotides –> cytopenia

137
Q

What would happen to blood CsA concentrations in a dog on cyclosporine who is given barbiturates?

A

Reduced CsA blood levels

138
Q

Is isotretinoin a first- or second-generation retinoid?

A

first (non-aromatic and do not act selectively on receptors)

139
Q

True or false: oral bioavailability of Vitamin A is improved with food intake.

A

True (it’s lipophilic)

140
Q

How is retinol transported in the serum?

A

Via retinol binding protein (RBP) + transthyretin

141
Q

What antibiotics may increase serum levels of retinoids?

A

Tetracyclines
Macrolides

142
Q

Is etretinate a first- or second-generation retinoid?

A

Second

143
Q

Is acitretin a first- or second-generation retinoid?

A

Second

144
Q

What labwork changes should be monitored with isotretinoin use?

A

Hypertriglyceridemia
Hypercholesterolemia
LE elevation

145
Q

What clinical side effects may be seen with isotretinoin use?

A

KCS/conjunctivitis
Pruritus
GI upset
Hyperactivity

146
Q

Which retinoids are ineffective in WHWT epidermal dysplasia?

A

Isotretinoin
Etretinate
Acitretin

147
Q

If choosing between Sandimmune and Neoral for a patient prescribed CsA, which would you prefer to use?

A

Neoral (microemulsion)

148
Q

What are the main cytokines affected by CsA?

A

IL-2* (less T-cell proliferation)
IL-3
IL-4* (less B-cell activation)
G-CSF (less neut release)
TNF-a*
IFN-gamma*
TGF-B (enhanced by CsA)

149
Q

What drugs can INCREASE CsA in the blood?

A

Azoles
Diltiazem
Doxycycline
Erythromycin
Methylpred

150
Q

What drugs can DECREASE CsA concentration in the blood?

A

Phenytoin
TMS
Phenobarb
Rifampin

151
Q

How does retinoid acid enter the cell nucleus?

A

Binds to either retinoic acid receptors or retinoid X receptors (RXRs)

152
Q

You have a choice between prescribing isotretinoin or acitretin to a patient. You want to avoid side effects as much as possible, which would you choose?

A

Etretinate (2nd gen=more selectivity and less potential for SE)

153
Q

What type of drug is pentoxifylline?

A

Methylxanthine derivative

154
Q

What cytokines are suppressed by pentoxifylline?

A

IL-1
IL-6
TNF-a

155
Q

What is the metabolite of hydroxyzine?

A

Cetirizine

156
Q

What drug is a natural metabolite of retinol?

A

Retinoic acid

157
Q

You want to prescribe a Basset hound a retinoid to help with seborrhea. Which retinoids would you AVOID?

A

Isotretinoin
Acitretin
(these are ineffective)

158
Q

What is the MOA of cyclophosphamide?

A

Alkylating agent that causes cross-linking of DNA

159
Q

What is the active metabolite of cyclophosphamide?

A

4-hydroxycyclophosphamide

160
Q

What metabolite of cyclophosphamide is responsible for causing sterile hemorrhagic cystitis?

A

acrolein (excrete in urine)

161
Q

Besides the liver, where else is CsA primarily metabolized?

A

Intestinal cells

162
Q

What is the suspected MOA of CsA-induced gingival hyperplasia?

A

Increased fibroblast activity and ECM deposition

163
Q

What is the effect of CsA on platelets?

A

Increased platelet synthesis of thromboxane A2 -> vasoconstriction and hypercoagulability

164
Q

What is the most reliable method of therapeutic drug monitoring of CsA?

A

High pressure liquid chromatography (HPLC)

165
Q

What is the primary antibody present in human IVIG?

A

IgG

166
Q

What TLR does imiquimod bind to?

A

TLR7

167
Q

What cytokines are secreted when imiquimod binds to TLR7?

A

IFN-a
IL-12
TNF-a

168
Q

What type of T-helper cell response dominates in a patient being treated with imiquimod?

A

Th1

169
Q

What is the MOA of leflunomide?

A

Converted into A77-1726 –> inhibits protein tyrosine kinase and dihydro-orotate dehydrogenase –> reduced pyrimidine synthesis –> reduced lymphocyte proliferation

170
Q

What are the main side effects of leflunomide?

A

LE elevations
Thrombocytopenia
GI upset
Lethargy
Hemorrhage

171
Q

What is the typical onset of action of Cytopoint?

A

1-3 days

172
Q

What amino acid is melatonin derived from?

A

Tryptophan

173
Q

What cytokines are decreased in response to oclacitinib?

A

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

174
Q

What drugs should you be cautious about using with melatonin?

A

Benzodiazepines

175
Q

What neurotransmitter can be transformed into melatonin?

A

Serotonin

176
Q

What is the expected effect of norepinephrine on melatonin synthesis?

A

It increases melatonin synthesis

177
Q

Does darkness inhibit or enhance melatonin synthesis?

A

Enhances

178
Q

What cytokines are produced in response to melatonin?

A

IL-2
IL-6
IL-12

179
Q

What T-cell subset is enhanced by melatonin?

A

CD4+ (T-helper)

180
Q

What T-helper response is promoted by melatonin?

A

Th2

181
Q

What is the effect of melatonin on GnRH secretion?

A

Inhibitor

182
Q

Where is mycophenolate metabolized?

A

Liver

183
Q

What enzyme turns mycophenolate into an inactive metabolite?

A

Glucuronyl transferase

184
Q

A dog is on an antacid and you want to prescribe it mycophenolate. What is an important consideration for the formula of mycophenolate used in this case?

A

Use an enteric-coated tablet (antacid will raise gastric pH and affect absorption of MMF)

185
Q

What JAK is primarily involved in hematopoiesis and myelopoiesis?

A

JAK2

186
Q

What immunomodulatory medication has been associated with fatal disseminated toxoplasmosis in an FIV+ cat?

A

Apoquel

187
Q

What is the active form of vitamin B3 called?

A

Niacinamide

188
Q

A client bought nicotinamide for their dog when you requested they purchase niacinamide. Is this okay to use?

A

Yes they are the same drug

189
Q

Describe the anti-inflammatory properties of tetracyclines.

A

Inhibit MMPs
Decrease IL-1, IL-6, IL-8, TNF-a
Suppress leukocyte chemotaxis via inhibition of MCP-1 and IL-8
Decrease IgE and histamine release
Inhibit phospholipase A2

190
Q

Describe the anti-inflammatory effects of niacinamide.

A

Stabilizes mast cells
Suppresses ICAM-1 expression
Suppresses MHC II expression
Inhibits phosphodiesterases
Inhibits nitric oxide synthase

191
Q

Which cytokines are reduced by niacinamide?

A

IL-1B
IL-6
IL-8
TNF-a

192
Q

Why would you recommend avoiding tetracyclines in young animals?

A

Slows fetal skeletal development
Discolors deciduous teeth

193
Q

Doxycycline is often given with food to reduce GI upset. Which foods should be avoided and why?

A

Calcium-containing products should be avoided as they will decrease the absorption of doxy (give 1-2 hours separate)

194
Q

Will antacids affect doxycycline use?

A

Yes - they will decrease its absorption so separate by 1-2 hours

195
Q

What is the MOA of 5-FU?

A

Pyrimidine analog –> binds to thymidylate synthase–> interferes with synthesis of thymidine and is mis-incorporated into DNA –> reduced DNA/RNA synthesis

196
Q

What are the active metabolites of 5-FU?

A

FUMP
FdUMP
FdUTP

197
Q

What are the indications for 5-FU?

A

Carcinomas
Osteosarcoma
HSA
TVT
MCT

198
Q

What species should not be treated with 5-FU?

A

Cats

199
Q

A dog is presented after ingesting a portion of his owner’s 5-FU tube. What are the likely side effects?

A

Hyperammonemia
Seizures
Diarrhea
(death likely)

200
Q

What is the MOA of colchicine?

A

alkaloid which binds to microtubule proteins –> alters cell function

201
Q

What processes are inhibited by colchicine?

A

Neutrophil chemotaxis
IL-1 production
Histamine release
Ig secretion
Degranulation of lysosomes
Collagen synthesis (stims collagenases)

202
Q

What are the side effects of colchicine?

A

GI upset
Neutropenia
Renal toxicity
Peripheral neuropathy

203
Q

What are the indications for colchicine in dogs?

A

EBA
Shar Pei fever

204
Q

What type of drug is dapsone?

A

Anti-mycobacterial antibiotic

205
Q

What is the antibacterial MOA of dapsone?

A

Competes with para-amino-benzoate for the active site of dihydropteroate synthetase –> inhibits folic acid synthesis

206
Q

Describe the anti-inflammatory properties of dapsone.

A

Decreases neutrophil chemotaxis
Decreases complement activation
Decreases lysosomal enzyme synthesis

207
Q

Why is dapsone use contraindicated in cats?

A

Fatal hemolytic anemia and neurotoxicity

208
Q

What are the primary SE of dapsone in dogs?

A

Hepatotoxicity
Anemia
Leukopenia

209
Q

What type of drug is hydroxychloroquine?

A

Aminoquinolone anti-malarial

210
Q

What TLR is inhibited by hydroxychloroquine?

A

TLR9

211
Q

In which canine conditions has hydroxychloroquine been utilized?

A

ECLE
GDLE

212
Q

Where are interferons metabolized?

A

Kidneys

213
Q

What is lomustine also known as?

A

CCNU

214
Q

What type of drug is CCNU?

A

nitrosurea alkylating agent

215
Q

What is the MOA of CCNU?

A

binds at the O-6 of guanine –> DNA cross-linking –> cytotoxicity

216
Q

What are the primary SE of lomustine?

A

Bone marrow toxicity> Hepatotoxicity

217
Q

What are the neoplastic indications for CCNU in dogs and cats?

A

CETL and non-epitheliotropic lymphoma
MCT
Histiocytic sarcoma

218
Q

How often is CCNU dosed in dogs?

A

q21-28 days

219
Q

What medication might you consider giving to a dog who is being treated with lomustine any why?

A

Denamarin – has a protective effect against CCNU-induced hepatotoxicity

220
Q

Where are CCNU antitumor metabolites produced?

A

Liver

221
Q

During what part of the cell cycle is methotrexate active?

A

S phase

222
Q

What is the MOA of vincristine?

A

Binds to tubulin –> disrupts mitotic spindle during mitosis

223
Q

What is the MOA of amphotericin B?

A

Binds to sterols (i.e. ergosterol) in plasma membrane –> pores form –> leakage of intracellular enzymes

224
Q

Besides ergosterol, what other component of the cell membrane can amphotericin B bind to (thus resulting in side effects)?

A

Cholesterol (binds to any sterols)

225
Q

How does amphotericin B lead to potential nephrotoxicity?

A

Binds to cholesterol in renal tubules and renal epithelial cells –> pores form –> nephrotoxicity

226
Q

What is the MOA of nystatin?

A

Binds to ergosterol in cell membrane –> pore forms –> leakage of intracellular ions

227
Q

Which is more toxic, nystatin or amphotericin B?

A

Nystatin (this is why it isn’t used systemically)

228
Q

What is the MOA of terbinafine?

A

Inhibits squalene epoxidase so that squalene cannot be converted to lanosterol (and therefore cannot be converted to ergosterol)

229
Q

What is the MOA of azoles?

A

Inhibit 14-a-demethylase so that lanosterol cannot be converted to ergosterol

230
Q

What is the MOA of echinocandins (i.e. caspofungin)?

A

Inhibit Beta-(1,3)-glucan synthase –> lack of formation of Beta-(1,3)-glucan in fungal cell wall

231
Q

What is the benefit of echinocandin antifungals over other antifungal drugs

A

Less potential for mammalian cell toxicity because Beta-(1,3)-glucan synthase is absent in mammalian cells

232
Q

What is the MOA of griseofulvin?

A

Binds to tubulin –> inhibits microtubule formation –> reduced fungal cell mitosis

233
Q

What is the MOA of flucytosine?

A

Converted to 5-FU –> acts as antimetabolite by competing with uracil –> inhibits pyrimidine metabolism –> reduced RNA and protein synthesis

234
Q

What is the antifungal MOA of lufenuron?

A

Disrupts chitin and chitosan synthesis in fungal cell walls

235
Q

What class of drug is amphotericin B?

A

Polyenes

236
Q

What class of drug is terbinafine?

A

Allylamines

237
Q

Is griseofulvin fungistatic or fungicidal?

A

Fungistatic

238
Q

What fungal organisms are the primary indication for griseofulvin?

A

Dermatophytes (ineffective against most other fungi)

239
Q

Should griseofulvin be given with or without food?

A

With (fatty meal)

240
Q

Is griseofulvin a cytochrome p450 inhibitor or inducer?

A

Inducer (increases metabolism of other p450 drugs)

241
Q

What antifungal has been associated with development of TEN and erythema multiforme?

A

Griseofulvin

242
Q

Is griseofulvin-induced myelotoxicity dose-dependent?

A

No, idiosyncratic

243
Q

What cat breeds may be more susceptible to griseofulvin-related idiosyncratic drug rxns?

A

Persians
Himalayans
Abysinnians
Siamese

244
Q

Why is flucytosine usually combined with amphotericin B?

A

High likelihood of resistance to flucytosine

245
Q

What fungal organisms are the primary indication for flucytosine use?

A

Aspergillus
Candida
Cryptococcus

246
Q

What enzyme is responsible for converting flucytosine to 5-FU?

A

Cytosine deaminase

247
Q

Why is flucytosine less toxic to mammalian cells than fungal cells?

A

Mammalian cells are lacking cytosine deaminase which is responsible for converting flucytosine to 5-FU

248
Q

What are the primary SE of flucytosine?

A

Myelosuppression
Nephrotoxicity
Cutaneous drug eruptions
GI upset
Hepatotoxicity
CNS signs

249
Q

A pregnant animal requires the use of a systemic antifungal medication. Which one is safe to use?

A

Terbinafine

250
Q

What class of drugs is nystatin?

A

Polyenes

251
Q

Besides fungi, what other organism is amphotericin B effective against?

A

Leishmania

252
Q

True or false: Amphotericin B is highly effective against dermatophytes

A

False

253
Q

Is amphotericin B fungistatic or fungicidal?

A

Fungicidal at high concentrations
Fungistatic at low concentrations

254
Q

What are the main SE of amphotericin B?

A

nephrotoxicity (cats more sensitive)
Non-regenerative anemia
Anorexia

255
Q

Through which mechanism do penicillins cause an adverse drug reaction?

A

Hapten hypothesis (B- and T-cells activated)

256
Q

What are the 4 mechanisms of drug allergy?

A

Hapten hypothesis
Danger theory
Pharmacological interaction concept
Viral reactivation

257
Q

What 2 drugs have been associated with pruritus as a CADR in cats?

A

Spironolactone
Methimazole

257
Q

What type of hypersensitivity is involved in pruritus caused by a CADR?

A

Type I
Type IV

258
Q

What type of hypersensitivity is urticaria and edema?

A

Type I

259
Q

What type of hypersensitivity is a PF-like CADR?

A

Type II

260
Q

What type of hypersensitivity is a vasculitis CADR?

A

Type III

261
Q

What type of hypersensitivity is a fixed drug eruption?

A

Type IV (cell mediated cytotoxic response)

262
Q

What %BSA is affected in an EM drug reaction?

A

<10%

263
Q

What type of hypersensitivity is Sweet’s syndrome?

A

Type IV

264
Q

What breed has been associated with superficial suppurative necrolytic dermatitis and what is the causative agent?

A

Miniature schnauzers
Natural shampoos

MK ACVD Exam (17 decks)

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