Pharmacology (1-24) Flashcards

1
Q

what does rINN stand for

A

recognised international non-prprietary name

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2
Q

what does BAN stand for

A

British Approved Name

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3
Q

what does USAN stand for

A

United States Approved Name

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4
Q

this determines what the body does to the drug (Absorption, Distrbution, Metabolism, Excretion)

A

pharmacokinetics

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5
Q

name the 4 parts of pharmacokinetics

A
  1. Absorption
  2. Distribution
  3. Metabolism
  4. Excretion
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6
Q

this is defined as what the drug does to the body / the relationship to drug concentration at the effect site

A

pharmacodynamics

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7
Q

name the pharmacokinetic model

helps understanding but is not directly relevant for clinical practice

A

one-compartment model

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8
Q

name the pharmacokinetic model

describes movement between compartments; drug is only removed from central compartment

A

two-compartment model

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9
Q

name the pharmacokinetic model

most commonly used to describe clinical scenarios

A

three-compartment model

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10
Q

name the pharmacokinetic model

drug is eliminated from the body, elimination occurs from central compartment

A

open model

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11
Q

name the pharmacokinetic model

drug is recirculated / drug is released into GIT via bile and then reabsorbed into plasma (enterohepatic recirculation)

A

closed model

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12
Q

reaction order?

rate at which drug concentration changes is constant and independent of drug concentration; rate of elimination is constant

A

zero order kinetics: 𝚫C/𝚫t = -K0

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13
Q

reaction order?

rate of drug elimination changes and is proportional to drug concentration; drug concentration decays exponentially; applies to most commonly used drugs

A

first order kinetics: 𝚫C/𝚫t = -KC

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14
Q

name 4 pH environments that may lead to ion trapping effect with drugs

A
  1. gastric pH
  2. fetal pH
  3. milk pH
  4. urine pH
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15
Q

what is the Henderson Hasselbach equation for acids

A

pH - pKa = log(ionized/nonionized)

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16
Q

what is the Henderson Hasselbach equation for bases

A

pH - pKa = log (nonionized/ionized)

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17
Q

how to find the pKa of a drug

A

pH at which 50% of the drug is ionized

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18
Q

this is the passage of a drug from site of administration to blood stream; influenced by solubility, physiochemical properties, site of administration, and bioavailability

A

absorption

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19
Q

name the 3 types of parenteral administration

A
  1. intravenous
  2. intramuscular
  3. subcutaneous
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20
Q

name the route of administration

most rapid onset of action, rate of administration usually slow

A

intravenous

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21
Q

name the route of administration

bypasses GIT, achieves sytemic levels more rapidly, advantageous when animal is inappetant or vomiting

A

parenteral

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22
Q

name the route of administration

often the only option for owners, influenced by speed of gastric emptying and presence of food

A

oral

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23
Q

this refers to the removal of a percentage of the drug as it passes through the liver via the portal vein before it reaches the systemic circulation and effect site

A

first pass effect

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24
Q

what effect does vasoconstriction have on absorption of agent from a site

A

reduces it

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25
Q

this is an indication of total exposure to the drug, used to define bioavailability, and used to calculate clearance

A

area under the curve (AUC)

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26
Q

this defines the extent to which an administered does of a drug enters the systemic circulation intact; referred to as F

A

bioavailability

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27
Q

what is the bioavailability of intravenous drugs

A

100%

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28
Q

this feature of pharmacokinetics is influenced by movement across membranes, blood flow to different organs, lipid solubility, and plasma protein binding

A

distribution

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29
Q

this is the main plasma protein drugs bind to

A

albumin

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30
Q

what is the equation for volume of distribution for a drug

A

Vd = Dose / C0

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31
Q

this is the peak plasma concentration after equilibrium is achieved and before elemination has begun

A

C0

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32
Q

this enhances drug access to sites of metabolism

A

lipid solubility

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33
Q

this enchances possibility of renal excretion of drug

A

water solubility

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34
Q

this part of drug elimination occurs mainly in the liver (but also in plasma, kidney, gut and lung); in phase 1 or phase 2 reactions

A

biotransformation

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35
Q

what are the 3 types of phase 1 biotransformation reactions?

A
  1. hydrolysis
  2. reduction
  3. oxidation
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36
Q

what are the 3 types of phase 2 biotransformation reactions

A
  1. acetylation
  2. glucoronidation
  3. conjugation to amino acids
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37
Q

what is the main organ for drug excretion?

A

kidney

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38
Q

what are the 3 main factors for drug excretion by the kidney

A
  1. water solubility
  2. GFR
  3. Active Transport
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39
Q

what are the 2 factors for reabsorption of a drug

A
  1. lipid solubility
  2. ionisation (ion trapping)
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40
Q

what are the 3 less common routes of drug elimination?

A
  1. biliary
  2. skin
  3. pulmonary
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41
Q

this is the time taken for the plasma drug concentration to fall by 50%

A

half-life of elimination

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42
Q

what is the equation for half-life in terms of K (slope of the PDC/time curve)

A

t 1/2 = 0.693 / K

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43
Q

name 3 factors affecting half-life of a drug

A
  1. access to sites of biotransformation or elimination
  2. interaction with other drugs
  3. physiologica/pthological states
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44
Q

what is the equation for the relationship between half-life and clearance?

A

t 1/2 = 0.693 x Vd / Cl_B

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45
Q

this is defined as the volume of blood cleared of the drug by all elimination processes per unit of time (mL/min) - encompasses biotransformation and excretion processes

A

clearance

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46
Q

this is where the levels of drug remain stable or consistent from dose to dose

A

steady state

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47
Q

how many half-lives does it take to reach 95% steady state

A

5

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48
Q

how many half-lives does it take to reach 99% steady state

A

7

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49
Q

name the 3 ways steady state can be achieved

A
  1. intravenous continuous infusion
  2. loading dose followed by a regular dose at fixed intervals
  3. fixed interval of a regular does
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50
Q

what is the fluctuation within steady state if the dose interval is the same as the half-life

A

50%

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51
Q

what is the fluctuation within steady state if the dose interval is twice the half-life

A

75%

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52
Q

name the formula for acids

(pharmacology summary of Formulae)

A

pH - PKa = log[ionized/non-ionized]

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53
Q

name the formula for bases

(pharmacology summary of Formulae)

A

pH - PKa = log[non-ionized/ionized]

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54
Q

name the formula for bioavailability

(pharmacology summary of Formulae)

A

F = AUC oral / AUC IV

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55
Q

name the formula for volume of distribution

(pharmacology summary of Formulae)

A

Vd = dose/C_0

(where C_0 = concentration at time 0)

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56
Q

name the formulas for half-life

(pharmacology summary of Formulae)

A

t 1/2 = 0.693/K
t 1/2 = 0.693 x Vd/Cl

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57
Q

name the formula for clearance

(pharmacology summary of Formulae)

A

Cl = Vd x K

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58
Q

name the formula for dose

(pharmacology summary of Formulae)

A

Dose = [Cmax] x Vd

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59
Q

this is a macromolecular structure with which the drug reacts; may be a protein, enzyme, nucleic acid, or less specific

A

drug receptor

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60
Q

this is a drug that binds to a physiological receptor and mimics the effect of the endogenous ligand

A

agonist

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61
Q

this type of agonist can achieve maximal response even if not all the receptors are occupied

A

full agonist

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62
Q

this type of agonist is incapable of achieving maximal response even if all the receptors are occupied

A

partial agonist

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63
Q

this is the tendency of the ligand (drug) to bind to the receptor

A

affinity

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64
Q

this is a term used to describe how good the drug is at eliciting a response

A

efficacy

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65
Q

this is a relative term that is often used to compare two drugs - comparing the concentration required to elicit the same response

A

potency

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66
Q

this is the concentration of the drug required to produce 50% of maximal response

A

EC 50

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67
Q

these drugs habe affinity but have no instrinsic activity & block the effect of the agonist

A

antagonist

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68
Q

name the type of antagonist

most important, effects are reversible/surmpuntable by increasing amount of agonist

A

competitive antagonist

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69
Q

name the type of antagonist

cannot be overcome by increasing amount of agonist; ex: Aspirin

A

non-competitive antagonist

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70
Q

at equilibrium, the number of receptors occupied by the drug is related to the concentration of the drug & described by this equation

A

Hill-Langmuir equation

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71
Q

this defines the capacity of a drug to preferentially produce one particular effect

A

selectivity

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72
Q

this is an absolute term; a drug with this tends to only act on one particular receptor type

A

specificity

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73
Q

this is the ratio of the dose giving an undesirable effect over the dose required to give the desired effect

A

therapeutic index

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74
Q

name 4 types of drug receptors

A
  1. ion chanell cell surface transmembrane receptor
  2. G protin couple receptor
  3. protein kinase
  4. cytosolic receptor
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75
Q

this type of drug receptor mediates action of a variety of proteins such as insulin

A

protein kinases

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76
Q

this is when a receptor is exposed to a ligand and the response reaches a peak then begins to fall off (despit the continued presence of ligand)

A

receptor desensitization

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77
Q

this is when receptors become internalized and degraded within the cell

A

receptor down-regulation

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78
Q

this is a term used to denote the rapid loss of responsiveness to a drug following intial dosing

A

tachyphylaxis

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79
Q

what are drug dosing regimens based on?

A

normal healthy individuals

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80
Q

name 4 things that may cause a dosing regimen to need individualization

A
  1. age
  2. species
  3. health status
  4. concurrent treatment
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81
Q

certain states of the animal may cause drug dose regimens to need individualization bc they may result in these 3 changes

A
  1. changes in Vd
  2. changes in plasma protein binding
  3. changes in metabolism
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82
Q

name 4 routes of ectotoxicity for ectoparasiticides

A
  1. incorrect disposal
  2. leakage from fish farms
  3. excretion in feces or urine
  4. topical products washed off
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83
Q

name the 5 points of the BSAVA/BVA/BVZA 5-point plan for responsible ectoparasiticide use

A
  1. educate clients to check & prevent parasites
  2. understand the risks
  3. risk-based prescribing
  4. ensure appropriate use & disposa
  5. record & monitor use
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84
Q

what is the mode of action for systemic macrocytic lactones?

(ectoparasiticide)

A

bind to glutamate & GABA-activated chloride channels

(leading to paralysis and death)

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85
Q

do systemic macrocytic lactones have repellent or knock-down activity?

A

no

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86
Q

name the two main groups of systemic macrocytic lactones

A
  1. Avermectins
  2. Milbemycins
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87
Q

what are the 2 main parasites that systemic macrocytic lactones act against

A
  1. Mites (Sarcoptiforms & Demodex & other)
  2. Fleas
    (NOT ticks)
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88
Q

what species are systemic macrocytic lactones used clinically for?

A

range of species

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89
Q

these are licensed for flea control in dogs and cats in the US; derived from Saccharopolyspora spinosa; selective for insects

A

Spinosyn macrocytic lactones

(Spinosad and Spinetoram)

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90
Q

what type of pyrethroid is Permethrin

A

type 1 (non alpha-cyano)

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91
Q

what type of pyrethroid is Cypermethrin, Deltamethrin, and Flumethrin?

A

type 2 (alpha-cyano)

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92
Q

what is the mode of action of Pyrethrins & Pyrethroids?

(ectoparasiticides)

A

affect voltage-gated sodium channels

(causing hyper-exciitability and death)

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93
Q

what species are Pyrethrins & Pyrethroids used clinically on?

A

dogs, small mammals, horses, farm animals, poultry

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93
Q

do Pyrethrins & Pyrethroids have repellent or knock-down activity?

A

yes, good

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94
Q

what adverse effects can type 1 Pyrethroids have?

A
  1. excitation
  2. tremors
  3. hyperthermia
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95
Q

what adverse effects can type 2 Pyrethroids have?

A
  1. salivation
  2. extensor tone
  3. incoordination
  4. seizures
  5. apnea
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96
Q

what is the mode of action for oxadiazines?

A

blocks neuronal sodium channels

(causing paralysis and death)

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97
Q

do oxadiazines have repellent or knowck-down activity?

A

no

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97
Q

what species are oxadiazines used for clinically?

A

dogs and cats

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98
Q

what is the mode of action for phenylpyrazoles?

(ectoparasiticide)

A

bind to GABA & glutamate-activated chloride channels

(leading to hyper-excitability and death)

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99
Q

name two types of phenylpyrazoles

(ectoparasiticide)

A
  1. fipronil
  2. pyriprole
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100
Q

what species are phenylpyrazoles used for clinically?

A

dogs and cats

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101
Q

does phenylpyrazoles have repellent or knowck-down activity?

A

no

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102
Q

which ectoparasiticide is topical and spreads in sebum?

A

phenylpyrazoles

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103
Q

what two species are phenylpyrazoles highly toxic to?

A

rabbits and fish

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104
Q

what is the mode of action for neonicotinoids?

(ectoparasiticide)

A

bind to nicotinic acetylcholine receptors

(leading to hyper-excitability, paralysis and death)

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105
Q

do neonicotinoids have repellent or knock-down activity?

A

no (except nitenpyram has knock-down effect)

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105
Q

what species are neonicotinoids used for clinically?

A

dogs, cats, small mammals

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106
Q

name 3 types of neonicotinoids

A
  1. nitenpyram
  2. imidacloprid
  3. dinotefuran
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107
Q

what is the mode of action for isoxazolines?

(ectoparasiticide)

A

bind to GABA and glutamate-activated chloride channels

(causing hyper-excitability and death)

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108
Q

what parasites are isoxazolines efficient on

A
  1. fleas and other insects
  2. Sarcoptes, Demodex & other mites
  3. ticks
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108
Q

do isoxazolines have repellent or knock-down activity?

A

NO

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109
Q

what species are isoxazolines used to treat clinically?

A

dogs, cats, poultry

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110
Q

what percent are isoxazolines passed out unchanged in feces?

A

80-90%

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111
Q

what is the mode of action for formamidines?

(ectoparasiticide)

A
  1. monoamine oxidase inhibitor
  2. octopamine receptor agonist
  3. Alpha2 receptor agonist

(causing increased nerve activity and death)

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112
Q

what parasties are formamidines effictive against?

A
  1. Sarcoptes, Demodex & other mites
  2. ticks
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113
Q

do formamidines have repellent or knock-down activity?

A

yes, good

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114
Q

what species are formamidines used to treat clinically?

A

small animals, farm animals

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115
Q

what 3 animals are formamidines contraindicated for?

A
  1. cats
  2. horses
  3. chihuahuas
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116
Q

what is the mode of action for carbamates and organophosphates?

A

form complexes with acetylcholinesterases

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117
Q

do carbamates and organophosphates have repellent or knock-down activity?

A

yes, rapid

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118
Q

name 5 adverse effects of muscarinic overstimulation from organophosphate poisoning

A
  1. Salivation
  2. Lacrimation
  3. Urination
  4. Defecation
  5. GI cramps
  6. Emesis

(SLUDGE)

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119
Q

name 4 adverse effects of nicotinic overstimulation from organophosphate poisoning

A
  1. Mydriasia Tachycardia
  2. muscle Weakness
  3. Twitching
  4. Fasciculation
    (high BP, paralysis)

(MT WTF)

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120
Q

which ectoparasiticide can cause irreversible chronic neurotoxicity from long term sub-clinical exposure (ataxia, paresis, paralysis)

A

carbamates and organophosphates

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121
Q

what species are calcium polysulfides and thiosulphates (lime sulphur) used to treat clinically

A

cats, horses, SA camelids

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122
Q

what parasites are calcium polysulfides and thiosulphates (lime sulphur) effective against in cats?

A
  1. Demodex gatoi
  2. Lynxacarus
  3. Notoedres
  4. Cheyletiella
  5. Trombicula
  6. lice
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123
Q

what parasites are calcium polysulfides and thiosulphates (lime sulphur) effective against in horses?

A
  1. Chorioptes
  2. lice
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124
Q

what parasites are calcium polysulfides and thiosulphates (lime sulphur) effective against in SA camelids?

A
  1. Chorioptes
  2. Sarcoptes
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125
Q

do calcium polysulfides and thiosulphates (lime sulphur) have repellent or knock-down effects?

A

NO

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126
Q

name 4 adverse effects of calcium polysulfides and thiosulphates (lime sulphur)

A
  1. skin irritatio
  2. malodorous
  3. yellow stains
  4. oral ulcers if ingested
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127
Q

name the topical ectoparasiticide formulation

hydrophobic polymers (resist wetting and degradation);
silicons oils and fatty acids (gradual release and diffusion);
can cause physical injury or skin irritation

A

collars

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128
Q

name the topical ectoparasiticide formulation

raid systemic absorption/diffusion through skin and coat; sebum may be important for diffusion;
can have aversion or irritation, effects on furniture and surfaces, and environmental impacts

A

spot-on or pour-on

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129
Q

name the topical ectoparasiticide formulation

good application and distribution, but more difficult to apply;
vulnerable to wetting and bathing;
disliked by animals;
increased risk of eye exposure, inhalation, and ingestion as well as human exposure

A

sprays and dips

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130
Q

this is an agent that kills microbes or inhibits their growth without damaging the host

A

antimicrobials

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131
Q

these are microbial products that kill or inhibit other micro-organisms

A

antibiotic

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132
Q

these are synthetic agents with activity against bacterial

A

antibacterial

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133
Q

name the type of resistance

lack of acticity due to inherent phenotype (e.g. lack of target, failure to penetrate cell wall, etc.)

A

inherent

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134
Q

name the type of resistance

mutations that confer resistance

A

chromosomal

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135
Q

name the type of resistance

resistance genes on mobile genetic elements (e.g. plasmids)

A

transferable

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136
Q

what are mycoplasmas resistant to?

A

beta-lactams

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137
Q

what are anaerobes resistant to?

A

aminoglycosides

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138
Q

what are aerobes resistant to?

A

metronidazole

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139
Q

this is the biggest driver of antimicrobial resistance

A

antimicrobial use

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140
Q

name 3 methicillin resistant staphylocci (MRS) organisms of concern

A
  1. S. pseudointermedius (MRSP)
  2. S. schleiferi (MRSS)
  3. S. aureus (MRSA)
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141
Q

name 2 multidrug resistant (MDR) cocci organisms of concern

A
  1. Streptococcus
  2. Enterococcus
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142
Q

name 2 other multidrug resistant (MDR) organisms of concern

A
  1. Pseudomonas
  2. Salmonella
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143
Q

what does nosocomial mean?

A

healthcare-acquired

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144
Q

name the 3 most common problems of vet-visiting dogs, cats and horses that tend do get antimicrobials but do not always require systemic antimicrobial treatment

A
  1. pruritis
  2. diarrhea
  3. respiratory conditions
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145
Q

name the 3 most important drivers for antimicrobial use in practice which should be addressed to change the practice culture and improve antimicrobial stewardship (AMS)

A
  1. vet prescribing behaviors
  2. interactions with clients
  3. practice norms
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146
Q

this describes the drug-host interaction
(bioavailability, penetration and clearance)

A

pharmacokinetics (PK)

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147
Q

this describes the drug-target interaction
(mode of action)

A

Pharmacodynamics

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148
Q

name 6 factors affecting PK/PD drug models

A
  1. poor bioavailability
  2. hypovolemic shock/poor perfusion
  3. renal/liver failure
  4. increased minimum inhibitory concentration (MIC)
  5. biofilm
  6. pus, debris, foreign material
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149
Q

this type of drugs are largely restricted to extracellular fluid (ECF);
fluid retention, IV fluid therapy, and/or increased renal clearance may necessitate higher doses to ensure therapeutic concentrations at the site of infection

A

hydrophilic (water soluble)

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150
Q

this type of drug penetrates tissues effectively and are less affected by changes in fluid dynamics and clearance

A

lipophilic (fat-soluble)

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151
Q

excellent, good, or poor tissue penetration?

Chloramphenicols
Fluoroquinolones
Minocycline
Doxycycline
Metronidazole
Rifampin

A

excellent

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152
Q

excellent, good, or poor tissue penetration?

Trimethoprim-sulfonamides
Lincosamides
Macrolides
Tetracyclines

A

good

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153
Q

excellent, good, or poor tissue penetration?

Beta-lactamase inhibitors
Penicillins
Cephalosporins
Aminoglycosides & aminocyclitols

A

poor

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154
Q

name 3 concentration dependent antimicrobials

A
  1. most fluoroquinolones
  2. aminoglycosides
  3. metronidazole
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155
Q

name 2 time dependent antimicrobials

A
  1. penicillins
  2. cephalosporans
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156
Q

name 3 antimicrobials with mixed effects for mode of action

A
  1. some fluoroquinolones
  2. lincosamides
  3. tetracyclines
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157
Q

what is the efficacy of concentration dependent antimicrobials

A

ratio peak concentration (Cmax) to MIC

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158
Q

what is the efficacy of time dependent antimicrobials

A

time above MIC

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159
Q

what is the efficacy of antimicrobials with mixed effects

A

total 24h exposure (area under curve)

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160
Q

what is the dosing for concentration dependent antimicrobials

A

max dose every 24h

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161
Q

what is the dosing for time dependent antimicrobials

A

appropriate dose every 8-12h

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162
Q

Bacteristatic or Bactericidal?

Lincosamides
Macrolides
Chloramphenicols
Tetracyclines
Trimethoprim
Sulphonamides

A

bacteriostatic

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163
Q

Bacteriostatic or Bactericidal?

Penicillins
Cephalosporins
Fluoroquinolones
Trimethoprim-sulphonamides
Aminoglycosides & aminocyclitols
Metronidazole

A

bactericidal

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164
Q

Bacteriostatic or Bactericidal drugs?

may be more effective in seriously immunocompromised patients

A

Bactericidal drugs

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165
Q

Bacteriostatic or Bactericidal drugs?

may result in less toxin release and toxic shock in staphylococcal and streptococcal infections

A

Bacteriostatic drugs

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166
Q

Bacteriostatic or Bactericidal drugs?

minimum bactericidal concentration (MBC) is much higher than the MIC

A

bacteriostatic drugs

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167
Q

Bacteriostatic or Bactericidal drugs?

minimum bactericidal concentration (MBC) is close or identical to the MIC

A

bactericidal drugs

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168
Q

what is the most serious adverse drug reaction (ADR)

A

hypersensitivity reactions

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169
Q

what breed has a bred-specific risk of adverse drug reactions to sulphonamides

A

Dobermans

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170
Q

name the main route of excretion for these drugs

Fluoroquinolones
Rifampicin
Doxycycline
Chloramphenicols

A

hepatic (liver)

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171
Q

name the main route of excretion for these drugs

Tetracyclines
Lincosamides
Macrolides
Fluoroquinolones
Metronidazole

A

mixed hepatic-renal

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172
Q

name 5 circumstances where cuture and ASTs (antimicrobial sensitivity tests) are necessary

A
  1. deep or complex infections
  2. unusual cilinal signs/cytology
  3. Rod bacteria
  4. if empirical treatment fails
  5. if AMR is more likely
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173
Q

in these tests: the zones of inhibition around each antimicrobial disc are compared to agreed breakpoints

A

Kirby-Bauer disc diffusion

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174
Q

in Kirby-Bauer disc diffusion tests, what shows that the infection is susceptible

A

zone of inhibition (ZI) exceeds the breakpoint

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175
Q

in Kirby-Bauer disc diffusion tests, what shows that the infection is resistant

A

zone of inhibition (ZI) is less than the breakpoint

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176
Q

these methods determine the lowest concentration of antimicrobial that inhibits bacterial growth

A

MIC methods

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177
Q

if MIC is (lower or higher?) than the breakpoint the infection is considered susceptible

A

lower

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178
Q

if MIC is (lower or higher?) than the breakpoint the infection is considered resistant

A

higher

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179
Q

the capital letters (‘S’ or ‘R’ or ‘I’) on a bacterial AST refer to this

A

the exact MIC

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180
Q

how to determine which antimicrobial is most effective from an AST

A

compare breakpoint:MIC ratio (want >1)

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181
Q

this breakpoint:MIC ratio means that the tissue concentration is only just sufficient enough to treat the infection and there is a risk of treatment failure

A

1

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182
Q

this breakpoint:MIC ratio means that the efficacy is less likely to be affected by factors that alter tissue concentration

A

> 1

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183
Q

these can be effective in surface and superficial infections & some focal deep infections

A

topical microbials and antibiotics

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184
Q

name some effective antimicrobials

A
  1. chlorohexidine
  2. manuka honey
  3. hypochlorous acid
  4. polihexanide
  5. bleach
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185
Q

these antimicrobials have well established breakpoints, efficacy and saftey;
appropriate for empirical treatment

A

first line antimicrobials

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186
Q

these antimicrobials have a concern for AMR;
they should only be used when there is culture evidence and/or PK/PD factors suggesting that first line drugs would not be appropriate

A

second line antimicrobials

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187
Q

these antibiotics are critically important andd AMR is of great concern;
they may not be licensed for use in animals;
breakpoint, efficacy and sfety data may be limited;
must only be used where no first or second line antibiotics are effective and topical antimicrobial therapy is not feasible or effective

A

third line antibiotics

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188
Q

what line are these antibiotics?

Penicillins
Ampicillin & amoxicillin
1st & 2nd gen. cephalosporins
Clindamycin & lincomycin
Tetracyclines
Trimethoprim-sulphonamides
Spiramycin
Metronidazole

A

first line antimicrobials

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189
Q

what line are these antimicrobials?

3rd gen. cephalosporins
Fluoroquinolones
Florfenicol (in cattle)

A

2nd line antimicobials

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190
Q

what line are these antimicrobials?

Aminoglycosides
Anti-Pseudomonas penicillins
Azithromycin & clarithromycin
3rd & 4th gen. cephalosporins
Chloramphenicol & florfenicol (in horses and small animals)
Rifampicin
Nitrofurantoin

A

3rd line antimicrobials

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191
Q

name the common antimicrobial combination

high tissue perfusion;
effective against gram- anaerobes, anaerobes, staphylococci and most gram+ aerobes (except streptococci)

A

Fluoroquinolone & Metronidazole

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192
Q

name the common antimicrobial combination

low tissue penetration;
effective against gram- aerobes, most anaerobes and gram+ aerobes

A

Aminoglycoside & Amoxicillin-clavulanate

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193
Q

name the common antimicrobial combination

mixed tissue penetration;
effective against gram- aerobes, most anaerobes & gram+ aerobes

A

Aminoglycoside & Lincosamides

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194
Q

name the common antimicrobial combination

Mixed tissue penetration;
effective against gram- aerobes, most anaerobes and gram+aerobes;
high potential for AMR

A

Fluroquionolone & Amoxicillin-clavulanate

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195
Q

name the 4 principles of prophylactic treatment

A
  1. select antimicrobial appropriate to the infection risk
  2. start treatment before procedure for adequate plasma and tissue levels
  3. repeat treatment to maintain tissue levels
  4. pot-op treatment continued only if necessary
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196
Q

this is the treatment of the whole group including infected and non-infected animals;
may be considered to prevent the spread of disease

A

metaphylaxis

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197
Q

what is the mode of action for penicillins

A

disrupt bacterial cell wall causing lysis (penicillin-binding proteins - PBP)

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198
Q

what bacteria are penicillins most active against

A

gram-pos bacteria

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199
Q

name 3 categories of penicillins

A
  1. narrow spectrum penicillins
  2. aminopenicillins
  3. anti-staphylococcal pennicillins
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200
Q

amoxicillin is often combined with this beta-lactamase inhibitor

A

clavulanic acid

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201
Q

some bacterial PBPs act as beta-lactamases to cleave the beta-lactam ring and inactivate this class of antibiotics

A

penicillins

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202
Q

name 3 types of beta-lactamase inhibitors

A
  1. clavulanic acid
  2. sulbactam
  3. tazobactam
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203
Q

name the antibiotic class

inhibit beta-lactamases and enhance activity for penicillins susceptible to these enzymes

A

beta-lactamase inhibitors

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204
Q

how are cephalosporins classed?

(antibiotic)

A

generations (1G, 2G, 3G, 4G)

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205
Q

what is the mode of action for cephalosporin antibiotics?

A

similar to penicillins (disrupt the bacterial cell wall causing lysis)

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206
Q

what bacteria type are Cephalosporins NOT active against

A

enterococci (limited against anaerobes)

207
Q

what is the mode of action for lincosamides and macrolides?

(antibiotics)

A

bind to 50S ribosome subunit to prevent protein synthesis

208
Q

name 2 types of lincosamides

(antibiotics)

A
  1. clindamycin
  2. lincomycin
209
Q

what type of bacteria are lincosamides and macrolides most effective against?

A

gram-positive bacteria

210
Q

what type of bacteria are lincosamides and macrolides NOT effective against?

A

gram-negative bacteria

211
Q

name 3 things resistance to lincosamides and macrolides is associated with

A
  1. modified ribosome binding site (erm genes)
  2. efflux pumps
  3. bacteria drug modification
212
Q

what is the mode of action for Trimethoprim-sulphonamide ?

(antibiotics)

A

block folic acid synthesis (required for purine and pyrimidine synthesis)

213
Q

name an adverse effect of trimethoprim-sulphonamide

A

very bitter - salivation and foaming (cats)

214
Q

what type of bacteria are trimethoprim-sulphonamides most effective against (moderate activity)

A

gram-positive bacteria

215
Q

what is the mode of action for fluorquinolones?

(antibiotics)

A

inhibit topoisomoerase II (DNA gyrase) in gram-neg bacteria

(disrupts DNA cleavage, reunion and super-coiling)

216
Q

what 3 things is resistance to fluoroquinolones associated with

(antibiotics)

A
  1. decreased cell permeability
  2. efflux pumps
  3. altered topoisomerases
217
Q

what is the mode of action for aminoglycosides

(antibiotics)

A

block protein synthesis at 30S ribosome subunit

218
Q

what type of bacteria are aminoglycosides most effective against

A

gram-neg bacteria

219
Q

list the 6 aminoglycosides in order of most to least efficacy

(antibiotics)

A

amikacin > tobramycin > gentamycin > neomycin = kanamycin > streptomycin

aktgnks

220
Q

what 2 things is resistance to aminoglycosides associated with

(antibiotics)

A
  1. modification of ribosome binding site
  2. efflux pumps
221
Q

this is an antibiotic closely related to aminoglycosides;
lack most of the systemic toxicity assoc. with aminoglycosides BUT chromosomal resistance can occur rapidly

A

aminocyclitols

222
Q

what is the mode of action for tetracyclines

(antibiotics)

A

block protein synthesis through 30S ribosome subunit

223
Q

name 5 types of tetracyclines

(antibiotics)

A
  1. tetracycline
  2. chlortetracycline
  3. oxytetracycline
  4. doxycycline
  5. minocycline
224
Q

name 3 things resistance to tetracyclines is associated with

(antibiotics)

A
  1. multiple genes for efflux
  2. ribosome binding
  3. drug modification
225
Q

what is the mode of action for chloramphenicols

(antibiotics)

A

disrupt protein synthesis through 30S and 50S subunits

226
Q

what type of bacteria are chloramphenicols most effective against

A

anaerobes

227
Q

what is resistance to chloramphenicols associated with

A

drug inactivating enzymes

228
Q

what is the major adverse effect of chloramphenicols

(antibiotics)

A

fatal aplastic anemia in humans

229
Q

what is the mode of action for metronidazole

(antibiotics)

A

disrupts DNA strands and inhibits repair enzyme (DNAase-1)

230
Q

what conditions are required for metronidazole to be effective?
what is the only type of bacteria metronidazole is effective against

A

anaerobic

231
Q

what is an adverse effect of metronidazole

(antibiotics)

A

bitter - inappetance and hypersalivation (cats)

232
Q

what is the mode of action for rifampicin

(antibiotics)

A

inhibits RNA polymerase and DNA transcription

233
Q

what type of bacteria is rifampicin NOT effective against

(antibiotics)

A

gram-negative

234
Q

what is an adverse effect of rifampicin

(antibiotics)

A

red-orange discoloration of bodily fluids

235
Q

what is the mode of action for nitrofurans

(antibiotics)

A

disrupts mRNA translation (from intracellular bacterial metabolism)

236
Q

what type of bacteria is nitrofurantoin NOT effective against

(antibiotics)

A

anaerobes

237
Q

what type of infection is nitrofurantoin (nitrofurans) restricted to and why

A

UTIs bc of rapid renal excretion

238
Q

what are 3 adverse effects of nitrofurans

(antibiotics)

A
  1. erythema
  2. pruritic
  3. oedema
    (also toxicity and carcinogenic potential)
239
Q

name 5 antibiotics that are limited to topical use only due to toxicity and PD/PK factors

A
  1. polymixin B
  2. bacitacin
  3. silver sulphadiazine
  4. fusidic acid
  5. mupirocin
240
Q

name the topical antibiotic

cationic agent: disrupts bacterial cell membrane phospholipids;
more effective against gram-neg bacteria;
resistance (decr. permeability) is uncommon;
inactivated by pus and debris

A

Polymixin B

241
Q

name the topical antibiotic

acts on gram-pos bacteria by inhibitng cell wall peptoglycan synthesis

A

bacitracin

242
Q

name the topical antibiotic

inhibits ribosomal activity and protein synthesis;
mainly active against gram-pos bacteria (staph, strep, corynebacteria);
NOT active against enterococci;
resistance associated with decreased ribosomal binding

A

fusidic acid

243
Q

name the topical antibiotic

blocks nucleic acid synthesis;
active against gram-pos bacteria

A

novobiocin

244
Q

name the topical antibiotic

inhibits RNA synthesis;
active against gram-pos bacteria (incl MRSP and MRSA) - narrow spectrum ;
resistance associated with mutations in target enzyme

A

mupirocin

245
Q

what is the initial treatment choice for most fungal infections?

A

Azoles (imidazoles and triazoles)

246
Q

what is the mode of action for azoles

(antifungal)

A

inhibit ergosterol synthesis disrupting fungal cell wall metabolism

247
Q

are azoles fungistatic or fungicidal?

A

fungistatic

248
Q

which azole’s absorption is not affected by food

(antifungal)

A

Fluconazole

249
Q

whih azole’s absorption is decreased with food

(antifungal)

A

voriconazole

250
Q

list the 4 main azoles in order from most well-tolerated to least well-tolerated in terms of adverse effects

(antifungal)

A

fluconazole > itraconazole = voriconazole > ketoconazole

FIVK

251
Q

what is the most common adverse effect of azoles

(antifungal)

A

GIT upset

252
Q

what is the mode of action for Allylamines (terbinafine)

(antifungal)

A

blocks ergosterol synthesis through inhibition of aqualene epoxidase

253
Q

are allylamines (terbinafine) fungistatic or fungicidal?

A

fungicidal

254
Q

what type of fungi are allylamines (terbinafine) effective against

A

dermatophytes

255
Q

is absorption of allylamines (terbinafine) affected by food?

(antifungal)

A

no

256
Q

how are allylamines (terbinafine) excreted

(antifungal)

A

hepatic metabolism

257
Q

name 2 common polyenes

(antifungal)

A

nyastatin and natamycin

258
Q

what is the mode of action for polyenes

(antifungal)

A

disrupt fungal cell membranes by occupying ergosterol binding sites

259
Q

are polyenes fungistatic or fungicidal

A

fungicidal

260
Q

what type of fungi are polyenes used for

A

superficial fungal infections only (Malassezia and Candida)

261
Q

what is the mode of action for griseofulvin

(antifungal)

A

inhibits mitosis, nucleic acid synthesis and cell wall metabolism

262
Q

is griseofulvin fungistatic or fungicidal?

A

fungistatic

263
Q

what type of fungi is griseofulvin mainly used for

A

dermatophytosis in horses

264
Q

name the antifungal

fungicidal;
poorly absorbed by GI tract so must be given parenterally;
dose-related nephrotoxicity

A

Amphotericin B

265
Q

name the antifungal

traditional antifungal treatment;
mode of action unclear;
used systemically and topically;
can cause GIT upsets, sialadenitis, and goitre

A

sodium or potassium iodide

266
Q

name the antifungal

blocks RNA synthesis;
synergy with amphotericin B for Cryptococcus and Candida;
NOT effective for dermatophytes;
renal excretion;
can cause GIT upsets, bone marrow suppression, hypersensitivity reactions, and neurological problems (cats)

A

flucytosine

267
Q

what is the mode of action for Acyclovir, Famiciclovir, Ixouridine, and Remdesivir?

(antiviral)

A

nucleoside analogues that inhibit DNA/RNA synthesis

268
Q

what is Acyclovir most commonly used alongside to increase anti-viral effect

(antiviral)

A

recombinent feline IFN-omega OR human IFN-alpha

269
Q

what s Famiciclovir used systemically for?

(antiviral)

A

FHV-1 infections

270
Q

what is ixouridine used to treat?

(antiviral)

A

topically in FHV-1

271
Q

what is Remdesivir used to treat and how long must it be given?

(antiviral)

A

FIP (give SQ or IV for over 12 weeks)

272
Q

what is the mode of action of amantidine?

(antiviral)

A

block M2 protein ion channels to prevent endocytosis

273
Q

what type of viruses is amantidine active against

(antiviral)

A

enveloped RNA viruses

274
Q

what is teh mode of action for L-lysine

(antiviral)

A

peptide, competitive inhibitor of arginine

275
Q

what is L-lysine used for in cats

(antiviral)

A

FHV-1

276
Q

name the interferon

active against many DNA and RNA viruses by direct inhibition of viral replication and stimulating anti-viral immunity;
used for FIV and FeLV in cats;
used for papilloma virus infections in dogs;
topical administration alongside acyclovir for FHV-1 keratitis

(antiviral)

A

recombinent human IFN-alpha

277
Q

name the interferon

used in cats and dogs for acute and chronic viral conditions (FeLV, FIP, FCV and canine parvovirus infection)

(antiviral)

A

recombinent feline IFN-omega

278
Q

name 2 mycobacterial derived immunomodulators

(antiviral)

A
  1. Bacille Calmett-Guerin (BCG)
  2. Regressin-V
279
Q

name the 4 nucleoside analogue DNA/RNA synthesis inhitors used in animals

(antiviral)

A
  1. acyclovir
  2. famciclovir
  3. idoxuridine
  4. remdesivir

AFIR

280
Q

name a peptide antiviral drug used in animals

A

L-lysine

281
Q

what does VMR stand for?

A

veterinary medicines regulations

282
Q

what does VMD stand for?

A

veterinary medicines directorate

283
Q

this is the executive agency of DEFRA;
they operate the licensing system for animal medicines with aim to safe guard public health, animal health and the environment

A

veterinary medicines directorate (VMD)

284
Q

this is a national surveillance scheme run by the VMD which aims to record and monitor reports of suspected adverse reactions to veterinary medicines in both animals and humans

A

SARSS (suspected adverse reaction surveillance scheme)

285
Q

this is designed to provide information on the work of the VMD, plans and results, as well as general developments on the controls on veterinary medicines; publish quarterly reports

A

MAVIS (Marketing Authorizations Veterinary Information Service)

286
Q

this governing body offers advice to the VMD on behalf of the Secretary of State, in respect of new and renewal marketing authorizations (MA), provisional MAs, variations to MAs and Animal Test Certificates (ATCs)

A

VPC (veterinary products committee)

287
Q

who should adverse drug reactions be reported to

A

veterinary medicines directorate (VMD)

(under SARSS)

288
Q

what 3 things make it ideal to use licensed veterinary products

A
  1. safety
  2. quality
  3. efficacy
289
Q

name the 6 steps involved in drug development

A
  1. pre-discovery
  2. discovery
  3. pre-clinical testing
  4. clinical trials
  5. licensing
  6. marketing
290
Q

name the 4 legally classified categories of veterinary medicines

A
  1. prescription only medicine - vet (POM-V)
  2. POM-vet, pharmacist, SQP (POM-VPS)
  3. non-food animal - vet, pharmacist, SPQ (NFA-VPS)
  4. authorized vet medicine-general sales list (AVM-GSL)
291
Q

name the legally classified category of veterinary medicine

Can be prescribed by a VS after clinical assessment of the animal or herd;
in this category if contains a new active ingredient, has safety issues, a narrow safety margin, due to government policy or because specialised veterinary knowledge required for its use

A

Prescription Only Medicine – Veterinarian (POM‐V)

292
Q

name the legally classified category of veterinary medicine

Can be prescribed by VS or SQP, No clinical assessment is required but the prescriber must be sure owner is competent to administer the product;
in this category if: it is used to reduce or prevent endemic disease in herds or flocks or individual animals, there is some risk for user, consumer, animal or environment, but users made aware by verbal or written advice

A

Prescription Only Medicine – Veterinarian, Pharmacist, SQP (POM‐VPS)

293
Q

name the legally classified category of veterinary medicine

Similar to POM‐VPS but must be for non‐food animals

A

Non‐Food Animal – Veterinarian, Pharmacist, SQP (NFA–VPS)

294
Q

name the legally classified category of veterinary medicine

No restrictions on its supply;
wide safety margin and specialist advice is not required

A

Authorised Veterinary Medicine – General Sales List (AVM‐GSL)

295
Q

this is an assessment of relevant clinical information, which may include an examination of the animal

A

“clinical assessment”

296
Q

which step of ‘the cascade’ ?

Veterinary medicine with a Marketing Authorisation valid in GB or UK wide for indicated species and
condition

A

step 1

297
Q

which step of ‘the cascade’ ?

Veterinary medicine with a Marketing Authorisation valid in NI for indicated species and condition

A

step 2

298
Q

which step of ‘the cascade’ ?

veterinary medicine with a Marketing Authorization valid in GB, NI or UK wide for a different species or condition

A

step 3

299
Q

which step of ‘the cascade’ ?

human medicine with a Marketing Authorization valid in GB, NI or UK wide OR an authorized vet med from outside the UK

A

step 4

300
Q

which step of ‘the cascade’ ?

extemporaneous preparation prepared by a vet, pharmacist or person holding an appropriate Manufacturer’s Authorization, located in the UK

A

step 5

301
Q

if the withdrawal period is not specified on a veterinary medicine, what should it be set at for eggs and milk

A

no less than 7 days

302
Q

if the withdrawal period is not specified on a veterinary medicine, what should it be set at for meat

A

not less than 28 days

303
Q

if the withdrawal period is not specified on a veterinary medicine, what should it be set at for meat from fish

A

not less than 500 degree days

304
Q

this is a means of defining the product, its dose and other relevant instructions

A

prescription

305
Q

what must a written prescription contain?

(10)

A
  1. Name, address and phone number of prescriber
  2. Credentials of the prescriber
  3. Name and address of the person receiving the prescription
  4. A description of animal
  5. Drug, dose and instructions (incl. withdrawal period)
  6. Note if prescribing under the cascade
  7. Date
  8. Written in indelible format
  9. Signed
  10. “For animals under my care”
306
Q

what does the abbreviation od mean in prescriptions

A

once daily (omni die)

307
Q

what does the abbreviation sid mean in prescriptions

A

once daily (semel in die)

308
Q

what does the abbreviation bd mean in prescriptions

A

twice daily (bis die)

309
Q

what does the abbreviation tid mean in prescriptions

A

three times daily (ter in die)

310
Q

what does the abbreviation qid mean in prescriptions

A

four times daily (quarter in die)

311
Q

what does the abbreviation pc mean in prescriptions

A

after food (post cibum)

312
Q

what does the abbreviation ac mean in prescriptions

A

before food (ante cibum)

313
Q

what does the abbreviation prn mean in prescriptions

A

when required (pro re nata)

314
Q

are controlled drugs regulated under the VMR (veterinary medicines regulation)?

A

no

315
Q

name the schedule of controlled drugs

Vets have no authority to possess or prescribe these except with special license from Home Office
(ex: cannabis and LSD)

A

schedule 1

316
Q

name the schedule of controlled drugs

Special requirements for requisition, prescribing, record keeping, storage and disposal;
Requisition in writing to the supplier signed by the VS;
Stored in a home office approved, locked receptacle;
Destroyed in presence of a person authorised by the Secretary of State
(Ex: morphine, ketamine, fentanyl, secobarbital)

A

schedule 2

317
Q

name the schedule of controlled drugs

Subject to the same prescription and requisition requirements as schedule 2, BUT do not need to keep a record in a register;
Most should be kept in a locked receptacle;
(ex: pentobarbital, phenobarbital, buprenorphine and midazolam)

A

schedule 3

318
Q

name the schedule of controlled drugs

Exempt from most of the restrictions of controlled drugs;
(ex: benzodiazepines and anabolic substances)

A

schedule 4

319
Q

name the schedule of controlled drugs

Certain preparations containing codeine, cocaine and morphine in less than specified amounts;
Exempt from most of the requirements except that invoices need to be kept for two years

A

schedule 5

320
Q

what 3 things must you record on obtaining a schedule 2 drug

A
  1. date
  2. name and address of supplier
  3. amount obtained
321
Q

what 4 things must you record on supplying a schedule 2 drug

A
  1. date
  2. name and address of person supplied
  3. vet’s name
  4. amount supplied
322
Q

how long are controlled drug prescriptions valid for?

A

28 days

323
Q

how long should incoming and outgoing transaction records of POM-V and POM-VPS drugs be kept for

A

5 years

324
Q

name the scheme

Some veterinary products can be marketed without a marketing authorisation and therefore are not required to prove safety, quality or efficacy (but must be manufactured to certain standards)

A

exemption scheme for small pet animals

325
Q

products including these 3 agents are not included in the exemption scheme for small pet animals

A
  1. antibiotics
  2. narcotics
  3. psychotropics
326
Q

how long is a prescription for medicated feedstuffs valid for

A

3 months

327
Q

name 5 categories of feed additives

A
  1. technological additives
  2. sensory additives
  3. nutritional additives
  4. zootechnical additives
  5. coccidostats and histomonostats
328
Q

these can be defined as a substance used to maintain animals in good health or favorably affect their performance

A

feed additives

329
Q

name 2 things the person supplied sheep dip must have one of

A
  1. Certificate of Competence in the Safe Use of Sheep Dips
  2. NPTC Level 2 Award in the Safe Use of Sheep Dip (QCF)
330
Q

name the 2 things that must be given to the purchaser if the sheep dip is an organophosphorous compound

A
  1. two pairs of heavy duty gauntlet style gloves
  2. A4 laminated safety notice
331
Q

name 4 features the permanent building for storing medicines must have

A
  1. secure
  2. clean
  3. vermin proof
  4. refridgerated space with temp monitoring
332
Q

these are monoamines derived from the amino acid tyrosine;
they are water soluble and 50% bound to plasma proteins in circulation;
include adrenaline, noradrenaline and dopamine

A

catecholamine transmitters

333
Q

these are drugs with similar actions to the postganlionic fibers of the SNS;
they resemble adrenaline in their actions and are also referred to as adrenergics

A

sympathomimetics

334
Q

these are drugs that oppose the actions of the postganglionic fibers of the SNS;
they are also referred to as antiadrenergics or sympathetic (adrenergic) antagonists

A

sympatholytic

335
Q

these are drugs that stimulate postsynaptic muscarinic receptors;
their actions resemble acetylcholine and they are also referred to as cholinergics or parasympathetic agonists

A

parasympathomimetics

336
Q

these are drugs that oppose the actions of the PNS at the muscarinic receptors by blocking the actions of acetylcholine;
also referred to as anticholinergics, parasympathetic antagonists or occasionally vagolytics

A

parasympatholytics

337
Q

adrenergic or cholinergic?

all presynaptic efferent autonomic fibers and the somatic motor fibers

A

cholinergic

338
Q

what do most postsynaptic sympathetic fibers release

A

noradrenaline

339
Q

what is the effect of the sympathetic nervous system on the heart?

A

increased activity (beta1)

(rate, strength, conduction)

340
Q

what is the effect of the sympathetic nervous system on blood vessels

A

vasoconstriction (alpha1 and alpha2)

341
Q

what is the effect of the sympathetic nervous system on the iris

A

dilation of pupil (mydriasis) (alpha1)

342
Q

what is the effect of the sympathetic nervous system on the bronchi?

A

relaxation (beta2)

343
Q

what is the effect of the sympathetic nervous system on the GIT

A

decreased activity (alpha1&2, beta1&2)

344
Q

what is the effect of the sympathetic nervous system on the adrenal medulla

A

secretion (adrenaline)

345
Q

name the 5 key features of neurotransmitter function that provide potential targets for pharmacologic therapy

A
  1. synthesis
  2. storage
  3. release
  4. binding to receptor
  5. termination of action of the transmitter and receptor effects
346
Q

what is the synthesis step of adrenergic neurotransmission?

A
  1. Tyrosine converted to Dopa by tyrosine hydroxylase
  2. Dopa converted to dopamine
347
Q

what is the storage step of adrenergic neurotransmission?

A
  1. dopamine transported into synaptic vessel by VMAT
  2. dopamine converted to NE in the vesicle
348
Q

what is the release step of adrenergic neurotransmission?

A
  1. action potential opens calcium channels
  2. fusion of vesicles with surface membrane using SNARE receptors and VAMP proteins
  3. release of NE
349
Q

what can block the release of noradrealine in adrenergic neurotransmission

A

botulinum toxin

(cleaves SNARE proteins in neurons)

350
Q

what can be used to block the reuptake of noradrenaline by the norepinephrne transporter (NET)

A

tricyclic antidepressants

351
Q

name the adrenergic receptor

contracts smooth muscles:
1. vasoconstriction
2. pyloric sphincter contraction (stomach)
3. urinary sphincter contraction
4. pupillary dilation (mydriasis)
5. positive ionotropic effect (myocardium)

(Gq)

A

Alpha1 receptors

352
Q

name the adrenergic receptor

Presynaptic nerve terminals:
1. inhibits norepinephrine release
2. inhibits ACh release
3. inhibits insulin release

(Gi)

A

Alpha2 receptors

353
Q

name the adrenergic receptor

Heart and Kidneys:
1. incr. heart rate
2. incr. cardiac contractility and stroke
3. incr. renin release

(Gs)

A

Beta1 receptors

354
Q

name the adrenergic receptor

Relaxes Smooth Muscles, liver, pancreas, eye:
1. bronchodilation
2. decr. gastric contraction
3. decr. intestinal peristalsis
4. urinary retention
5. liver: glycogen to glucose
6. vasodilation

(Gs)

A

Beta2

355
Q

name the adrenergic receptor

Adipose Tissue:
1. sdipose tissue lipolysis
2. decr. urination

(Gs)

A

Beta3 receptors

356
Q

what is the effect of the parasympathetic nervous system on the heart

A

decr. activity

(M2 > M3)

357
Q

what is the effect of the parasympathetic nervous system on the blood vessels

A

vasodilation

(M2)

358
Q

what is the effect of the parasympathetic nervous system on the iris

A

contraction of pupil (myosis)

(M2, M3)

359
Q

what is the effect of the parasympathetic nervous system on the bronchi

A

constriction

(M2 = M3)

360
Q

what is the effect of the parasympathetic nervous system on the GIT

A

incr. activity

(M2=M3)

361
Q

what is the effect of the parasympathetic nervous system on the adrenal medulla

A

no effect

362
Q

what is the synthesis step of cholinergic neurotransmission

A
  1. choline transported into presynaptic nerve terminal
  2. ACh synthesized from choline and acetyl CoA by choline acetyltransferase (ChAT)
363
Q

what is the storage step of cholinergic neurotransmission

A
  1. ACh transported into large, clear vesicles by VAT along with neuropeptides and ATP
364
Q

what is the release step of cholinergic neurotransmission

A
  1. voltage sensitive Ca2+ channels open
  2. influx of Ca2+
  3. fusion of vesicles with surface membrane (involves SNAPs and VAMPs)
  4. expulsion of ACh and co-transmitters into synaptic cleft
365
Q

what can the release of ACh from the nerve terminal be blocked by

A

botulinum toxin

366
Q

how many muscarinic receptors are there

A

5 (M1-M5)

367
Q

what do muscarinic receptors M1, M4, and M5 act on

A

CNS

368
Q

what does muscarinic receptor 2 act on

A

heart (reduces HR)

369
Q

what does muscarinic receptor 3 act on

A

smooth muscle (contract)

370
Q

which cholinergic receptor?

blocked by curare;
linked to ion channels;
response is fast and brief;
located at neuromuscular junctions and autonomic ganglia;
mediate excitation in target cells;
post-synaptic

A

nicotinic

371
Q

which cholinergic receptor?

blocked by atropine;
linked to G-couple proteins;
found in smooth muscle;
mediate excitation and inhibition in target cells;
both pre- and postsynaptic

A

muscarinic

372
Q

name 3 possible mechanisms of drugs acting on the autonomic nervous system

A
  1. act on neurotransmitter receptor
  2. interfere with NT biosynthesis
  3. interfere with degradation of NT
373
Q

what do direct acting agonists or antagonists act on

(adrenergic drugs)

A

one or more postsynaptic adrenergic receptors (alpha1&2, beta1&2)

374
Q

name the type of adrenergic drug

increase release of NE or inhibit reuptake or block metabolising enzyme

A

indirect acting agonists

375
Q

name 2 ways a drug acting on the ANS can interfere with degradation of neurotransmitter

A
  1. inhibit degradation enzyme
  2. inhibit neurotransmitter reuptake
376
Q

name 2 ways a drug acting on the ANS can interfere with neurotransmitter biosynthesis

A
  1. inhibit precursor uptake
  2. inhibit enzyme for biosynthesis
377
Q

what are the ACh receptors

A

nicotinic and muscarinic

378
Q

what are teh 3 main types of nicotinic receptors

A
  1. muscle (NMJ)
  2. ganglionic (ANS)
  3. CNS (brain)
379
Q

name the 4 main classes of drugs affecting PNS

A
  1. Muscarinic agonists (parasympathomimetics)
  2. muscarinic antagonists (anticholinergics)
  3. nicotinic agonists
  4. nicotinic antagonists (ganglion blockers)
380
Q

name 4 choline ester drugs (direct muscarinic agonists)

(parasympathomimetics)

A
  1. ACh
  2. Methacholine
  3. Bethanecol
  4. Carbachol
381
Q

what receptor do choline esters have a direct action on?

A

muscarinic receptors

382
Q

name the choline ester drug (muscarinic agonist - parasympathomimetic)

mainly muscarinic;
used inhaled for bronchial reactivity diagnosis

A

methacholine

383
Q

name the choline ester drug (muscarinic agonist - parasympathomimetic)

long acting;
highly specific for muscarinic receptors;
minimal cardiac negative chronotropic and ionotropic effects;
used to induce urination

A

bethanechol

384
Q

name the choline ester drug (muscarinic agonist - parasympathomimetic)

long acting;
significant nicotinic action;
used to induce gastric motility and urination and tpically to induce miosis

A

carbachol

385
Q

name 3 types of alkaloid drugs (direct muscarinic agonists)

(parasympathomimetics)

A
  1. pilocarpine
  2. muscarine
  3. arecoline
386
Q

name the alkaloid drug (muscarinic agonist - parasympathomimetic)

dominant muscarinic activity;
tertiary amine alkaloid, so increased lipid solubility;
added topically to the eye to induce miosis;
used for treatment of glaucoma;
contraindicated in uveitis and anterior lens luxation

A

pilocarpine

387
Q

these are indirectly acting parasympathomimetics;
they inhibit AChE to incr. ACh activity;
have a cholinergic effect initially but prolonged depolarization may have desensitization

A

anticholinesterases

388
Q

name 3 factors that contribute to the effects/toxicity of anticholinesterases

(indirect parasympathomimetics)

A
  1. reversible or irreversible
  2. affinity for receptor
  3. how readily they can access receptor (volatility and lipid solubility)
389
Q

name the 6 cholinergic effects of anticholinesterases that may lead to toxicity if in excess

(indirect parasympathomimetics)

A
  1. Salivation
  2. Lacrimation
  3. Urination
  4. Defecation
  5. Gastrointestinal distress
  6. Emesis

(SLUDGE)

390
Q

what are the 3 main uses of anticholinesterases?

(indirect parasympathomimetics)

A
  1. diagnosis of myasthenia gravis
  2. in anaesthesia to reverse neuromuscular blockade
  3. in connection with eye and GIT
391
Q

name the anticholinesterase (indirect parasympathomimetic)

very short acting quaternary ammonium compound;
reversal of non-depolarizing muscle relaxants;
diagnosis of myasthenia gravis

A

Edrophonium chloride ‘tensilon’

392
Q

name the anticholinesterase (indirect parasympathomimetic)

moderate duration of action;
reversal of non-depolarizing muscle relaxants;
treatment of myasthenia gravis (orally: TID, dose reduced as required)

A

Neostigmine

393
Q

name the anticholinesterase (indirect parasympathomimetic)

moderat duration;
more lipid soluble;
treatment of myasthenia gravis (orally: BID)

A

Pyridostigmine

394
Q

name the anticholinergic drug (muscarinic antagonist)

lipid soluble (crosses BBB);
used to increase HR and with anticholinesterases to prevent side effects from muscarinic stimulation;
not recommended in horses and rabbits are resistant;

A

atropine

395
Q

name the anticholinergic drug (muscarinic antagonist)

naturally ocurring agent;
crosses BBB - sedation;
used for drying secretions;
has antemetic properties;
contained in antispasmodic Buscopan with dipyrone metamizole

A

scopolamine (aka hyoscine)

396
Q

name the anticholinergic drug (muscarinic antagonist)

synthetic agent;
does not cross placenta or BBB;
less tachycardia;
slower onset and longer duration;
used to prevent and treat bradycadia (anaesthesia, vagal stimulation);
less CNS effects

A

Glycopirrolate

397
Q

name the anticholinergic drug (muscarinic antagonist)

bronchodilation in horses (R.A.O.);
inhalation - poor absorption therefore minimal side effects

A

Ipratopium bromide

398
Q

name the anticholinergic drug (muscarinic antagonist)

mydriatic and cycloplegic;
long duration of action

A

cyclopentolate

399
Q

name the anticholinergic drug (muscarinic antagonist)

used as a mydriatic (NOT cycloplegic);
drug of choice for intra-occular exam;
rapid acting, shorter duration of several hours

A

tropicamide

400
Q

name 3 naturally occuring catecholamines

(sympathomimetics)

A
  1. adrenaline
  2. noradrenaline
  3. dopamine
401
Q

name the sympathomimetic drug

non-selective: acts at both alpha- and beta-adrenoceptors;
effects: incr. HR, incr. force of contraction, vasocontriction;
used for cardiac arrest and anaphylaxis;
can induce tachycardias and arrhythmias

A

adrenaline

402
Q

name the sympathomimetic drug

alpha effects > beta1 effects > beta2 effects;
primarily a vasopressor via alpha stimulation;
used to treat hypotension

A

noradrenaline

403
Q

name the sympathomimetic drug

acts at dopamine receptors alpha- and beta-adrenoceptors;
dose dependent effect;
mixed effects in practice;
used to treat hypotension

A

dopamine

404
Q

what is the effect of dopamine at low doses

A

dopa effects:
1. vasodilation
2. incr. renal perfusion and filtration

405
Q

what is the effect of dopamine at medium doses

A

beta effects:
positive inotropy and chronotropy

406
Q

what is the effect of dopamine at high doses

A

alpha effects:
vasoconstriction

407
Q

name the sympathomimetic drug category

induces vasoconstriction and can increase the force of myocardial contraction;
includes phenylephrine and methoxamine

A

alpha1 agonists

408
Q

name the sympathomimetic drug

alpha1 agonist;
used in ocular preparations to induce mydriasis;
used in anaesthesia to increase arterial pressure;
used following anaesthesia in horses as nasal spray to cause vasoconstriction and reduce nasal congestion

A

phenylephrine

409
Q

name the sympathomimetic drug category

extensively used in vet med for their sedative nd analgesic properties;
CV effects: incr. SVR leading to reflex bradycardia;
includes: dexmedetomidine, medetomidine, xylazine, detomidine, romifidine

A

alpha2 agonists

410
Q

name the sympathomimetic drug

Beta1:
in equine anaesthesia to maintain mean arterial pressure;
used in SA for inotropic support in acute cardiac crisis;
short half life and rapid metabolism;
beta1 > beta2 > alpha1

A

Dobutamine

411
Q

name the sympathomimetic drug

beta2 agonist;
used in treatment of R.A.O. in horses;
can induce vasodilation;
growth promoting effect: hypertrophy of muscle fibers, protein deposition and lipolysis in adipose cells

A

Clenbuterol

412
Q

what are the 2 main effects of beta2 agonists?

(sympathomimetics)

A

bronchodilation and uterine relaxation

413
Q

name the sympathomimetic drug

beta2 agonist;
used in equine anaesthesia to treat hypoxemia due to V/Q mismatch;
can produce tachycardia

A

Salbutamol

414
Q

name the sympathomimetic drug

beta2 agonists;
used as a bronchodilator;
more cardiac side effects;
can be used to treat hyperkalemia

A

Terbutaline

415
Q

name the sympathomimetic drug

beta2 agonists;
used in the treatment of navicular disease;
induces vasodilation;
used as a tocolytic drug (decr. uterine contraction and delay parturition)

A

isoxuprine

416
Q

name the sympathomimetic drug

mixed effects on alpha and beta;
direct and indirect actions;
prone to tachyphylaxis;
used as a bolus to treat hypotension under GA

A

ephedrine

417
Q

name the sympathomimetic drug

alpha1-agonist properties (direct) and triggers noradrenaline release (indirect);
used for treatment of urinary incontinence in dogs;
has been used as a nasal decongestant

A

Phenylpropanolamine

418
Q

name the adrenoceptor antagonist drug

alpha1 antagonist:
highly selective;
produces vasodilation;
used in treatment of certain urinary tract conditions

A

Prazosin

419
Q

name the adrenoceptor antagonist drug

non-selective alpha antagonist:
irreversible, long-acting alpha-antagonist;
predominant alpha1-adrenoceptor blocking effect;
uses: pheochromocytoma stabilization, laminitis

A

Phenoxybenzamine

420
Q

name the adrenoceptor antagonist drug

non-selective alpha antagonists:
competitive, short acting;
predominant, alpha1-adrenoceptor blocking effect;
used to treat hypertensive crises;
can cause insulin secretion, leading to hypoglycemia

A

Phentolamine

421
Q

name the 4 cardinal signs of inflammation

A
  1. redness
  2. heat
  3. swelling
  4. pain (loss of function)
422
Q

name 4 benefits of inflammation

A
  1. incr. blood flow to injured tissue
  2. oedema formation (dilution effect)
  3. attraction of leukocytes and macrophages
  4. antibody production at site of infection
423
Q

name the 4 main uses of anti-inflammatory drugs (control of adverse effects of inflammatory response)

A
  1. analgesia (acute and chronic)
  2. anti-pyretic
  3. anti-endotoxic effect
  4. anti-thrombotic effect
424
Q

name the inflammatory mediator

released from mast cells, basophils, eosinophils;
causes vasodilation, incr. vascular permeability

A

histamine

425
Q

name the inflammatory mediator

originates from plasma, formed from kininogen by factor XII;
causes vasodilation, pain mediator

A

bradykinin

426
Q

name the inflammatory mediator

produced by many cell types;
causes gastroprotection, renoprotection, inflammation, reduction of pain threshold

A

prostaglandins (PGF2alpha, PGD2, PGE2)

427
Q

name the inflammatory mediator

produced by platelets;
causes platelet aggregation, vasoconstriction

A

thromboxanes (TXA2)

428
Q

name the inflammatory mediator

produced by platelets, mast cells;
cause incr. vascular permeability

A

Leukotrienes (LTB4)

429
Q

name the inflammatory mediator

produced by WBC, mast cells;
causes platelet aggregation, adherence of leukocytes to endothelium, lysosomal enzyme release

A

platelet aggregating factor

430
Q

name the inflammatory mediator

produced by plasma proteins;
cuase chemotaxis, opsonization

A

complement

431
Q

name the inflammatory mediator

produced by macrophages and mast cells;
cause initiation of inflammation and chemotaxis, pain mediator

A

cytokines

432
Q

name the inflammatory mediator

produced by mast cells and platelets;
cause vasoconstriction

A

5-HT

433
Q

name the 2 broad groups of NSAIDs

A
  1. enolic acids
  2. carboxylic acids
434
Q

what is the mechanism of action for NSAIDs?

A

inhibit cyclo-oxygenase (COX) enzyme 1 and/or 2

435
Q

which COX?

contitutive, constant production;
produce PGs involved in normal physiological processes

A

COX1

436
Q

which COX?

inducible, produced by inflammatory cells;
produce PGs invlved in inflammation

A

COX2

437
Q

name 2 NSAIDs which lead to an increased bleeding time

A

aspirin and ketoprofen

438
Q

name 2 NSAIDs which do NOT lead to increased bleeding time

A

meloxicam and carprofen

439
Q

where are NSAIDs absorbed well

A

stomach

440
Q

is metabolism and excretion of NSAIDs in young animals faster or slower?

A

slower

441
Q

what order of kinetics do most NSAIDs display?
(incr. concentration, faster clearance)

A

first order kinetics

442
Q

name 5 adverse side effects of NSAIDs (related mainly to inhibition of COX1)

A
  1. GI ulceration
  2. nephrotoxicity
  3. hepatotoxicity
  4. coagulation effects
  5. wound healing
443
Q

what species is paracetamol contraindicated in?
they have reduced levels of glutathione, so a much lower toxic dose

A

cats

444
Q

name the NSAID

alternatice mechanism of action (COX1, COX2, myeloperoxidase inhibitor);
good anitpyretic and analgesic, poor anti-inflammatory;
metabolism: glucoronidation, conjugaton, N-hydroxylation;
glutathione binds toxic metabolites which would otherwise cause hepatic necrosis

A

paracetamol

445
Q

name the NSAID

COX2 selective;
licensed in dogs, cats, horses, cattle, pigs, guinea pigs;
uses: acute and chronic musculoskeletal disorders, postoperative surgical pain, perioperative use;
do NOT use in prgnant or lactating animals OR animals < 6 weeks of age OR cats < 2kg

A

meloxicam

446
Q

name the NSAID

COX2 selective;
licensed in dogs, cats, cattle, horses;
uses: postoperative soft tissue/orthopedic pain, OA, perioperative use;
animals < 6 weeks have additional risk

A

carprofen

447
Q

name the NSAID

COX2 selective;
dogs and cats;
uses: peri and postoperative use, ST and orthopedic pain, OA;
safety NOT established in pregnancy/lactation, cats <4mo, dogs <2mo, or animals <2.5kg

A

Robenacoxib

448
Q

name the NSAID

COX2 selective;
dogs, horses;
uses: postoperative analgesia, OA;
cotraindications: pregnancy and lactation

A

firocoxib

449
Q

name the NSAID

COX2 selective;
dogs;
long term analgesia for OA in dogs;
contraindications: <12mo, < 5 kg

A

Mavacoxib

450
Q

name the NSAID

COX2 selective;
dogs;
uses: peri and postoperative pain due to orthopedic and soft tissue surgery, OA;
contraindications: <10 weeks, pregnancy and lactation

A

Cimicoxib

451
Q

name the equine NSAID

anti-inflammatory > analgesic;
COX1 and COX2;
concentrates in inflammatory exudate;
toxicity: PLE;
not for use in food-producing horses

A

Phenylbutazone aka “Bute”

452
Q

name the equine NSAID

prodrug, metabolized to phenylbutazone in liver;
more palatable, reduced GI ulceration;
expensive

A

Suxibuzone “Danilon”

453
Q

name the equine NSAID

analgesic dose and “anto-endotoxic” dose;
injectable, use in colic/ST or orthopedic pain

A

Flunixin

454
Q

name the equine NSAID

oral paste licensed for ST or orthopedic pain, preoperative use;
COX2 > COX1 ;
licensed in pregnancy;
has food withdrawal

A

Vedaprofen

455
Q

name the farm animal NSAID

name 3 farm animal NSAIDs

A
  1. flunixin
  2. meloxicam
  3. ketoprofen
456
Q

name the novel drug

non-COX inhibiting, specific prostaglandin receptor antagonist;
specifically targets EP4 receptor therefore minimal side effects;
long-term pain control for OA;
expensive

A

Grapiprant

457
Q

name 3 NSAIDs licensed for perioperative use

A
  1. meloxicam
  2. carprofen
  3. robenacoxib
458
Q

what are endogenous corticosteroids produced by

A

adrenal cortex

459
Q

what are the 2 categories of endogenous corticosteroids

A
  1. mineralocorticoids
  2. glucocorticoids
460
Q

what a re endogenous corticosteroids synthesized from

A

cholesterol

461
Q

where are corticosteroids metabolized

A

liver

462
Q

what is the active form of cortisone

A

cortisol

463
Q

what is the active form of prednisone

A

prednisolone

464
Q

what 4 types of effects do corticosteroids have

A
  1. metabolic effects
  2. systemic effects
  3. anti-inflammatory effects
  4. immune suppressive effects
465
Q

what type of effect do low doeses of corticosteroids have

A

physiological

466
Q

what type of effect do medium doeses of corticosteroids have

A

anti-inflammatory

467
Q

what type of effect do high doeses of corticosteroids have

A

immune suppressive

468
Q

name 5 systemic effects of corticosteroids

A
  1. elevated liver enzymes (dogs)
  2. alteration of CNS function
  3. PU/PD
  4. incr. appetite
  5. muscle wastage
469
Q

what do corticosteroids inhibit for effective anti-inflammatory action

A

inhibit PLA2 (entire AA pathway)

470
Q

name 7 adverse effects of corticosteroids

A
  1. gastric ulceration
  2. PU/PD
  3. hyperglycemia
  4. muscle atrophy
  5. osteoporotic effect
  6. Cushing’s disease
  7. suppression of HPA axis
471
Q

name 3 short acting (<24h) glucocorticoids

A
  1. predisolone
  2. Prednisone
  3. Methylprednisolone
472
Q

name 3 long acting (>24h) glucocorticoids

A
  1. dexamethasone
  2. betamethasone
  3. triamcinolone
473
Q

name the corticosteroid

parenteral formulation;
water soluble salts, ideal for IV administration

A

Dexamethasone

474
Q

name the corticosteroid

parenteral formulation;
insoluble esters, long acting, IM administration

A
  1. methylprednisolone acetate
  2. dexamethasone phenylproprionate / isonicotinate
475
Q

name 5 clinical uses of corticosteroids

A
  1. anti-inflammatory
  2. immune-mediated disease
  3. neoplasia
  4. treatment for hypoadrenocorticism
    5n. septic shock
476
Q

name 3 clinical uses of corticosteroids in farm animals

A
  1. termination of pregnancy / induce parturition
  2. acute trauma, neuropathies
  3. chronic resp. disease
477
Q

what are the two most commonly used classes of anthelmintic drugs in small animal practice

A
  1. Benzimidazoles
  2. Macrocylic lactones
478
Q

what do all Benzimidazole drugs licensed for dogs and cats contain (or its prodrug)

(anthelmintics)

A

fenbedazole (febental)

479
Q

name the small animal anthelmintic class

given orally, poorly absorbed from GIT (enhanced with food);
inhibit nematode tubulin polymerization and prevent microtubule formation affecting cellular transpot and energy metabolism;
metabolized in liver and mostly excreted in feces (small amount in urine and milk);
broad spectrum of action agaist nematodes in GIT and resp. tract (both adult and immature);
will treat Giardia;
limited action against cestodes

A

Benzimidazoles

480
Q

what are the two classes of Macrocyclic lactones

(anthelmintics)

A
  1. Avermectins
  2. Milbemycins
481
Q

name the small animal anthelmintic class

topical or oral admin;
accumulate in fat so long duration of action;
act on glutamate-gated chloride channels in nerve cells (paralysis);
narrower safety margin in cats;
largely excreted in feces and urine (small amount in milk);
topical products removed by bathing or swimming (harmful to aquatic life);
effective against wide range of nematodes in larval, immature and adult stages;
no activity against cestodes;
some can be used against Diofilaria

A

Macocytic lactones

482
Q

name the small animal anthelmintic

available as a spot on preparation for cats only in combination with ectoparasiticides and praziquantel;
slow absorption;
will treat GI nematodes, hookworm and capillaria;
effective against D. immitis larvae but not adults

A

Eprinomectin (Avermectin)

(Macrocyclic lactone)

483
Q

name the small animal anthelmintic

available for both cats and dogs;
applied topically, bathing will not affect efficacy after 2h drying time;
will treat roundworms, hookworms and prevent D. immitis;
some reports of salivation or vomiting in cats after licking site & of alopecia at site

A

Selamectin (Avermectin)

(Macrocyclic lactone)

484
Q

name the small animal anthelmintic

administered orally and largely excreted unchanged in feces;
any that is absorbed will be excreted in bile;
absorbed quickly but eliminated rapidly;
treats GI roundworms, hookworm and whipworm;
can be used as lungworm treatment or prevention

A

Milbemycin

(Macrocyclic lactone)

485
Q

what is the available drug for small animals in the Tetrahydropyrimidines class of anthelmintics

A

Pyrantel

486
Q

name the small animal anthelmintic

act on nicotinic acetylcholine receptors to initially cause muscle contraction and then paralysis;
giving with food will delay absorption;
max concentration achieved is more important than duration of exposure for effectiveness;
effective against adult and larval stages of GI nematodes;
can be used in puppies and kittens and during pregnancy

A

Pyrantel

(Tetrahydropyrimidines)

487
Q

name the small animal anthelmintic

acts at neuromuscular junction to stimulate presynaptic secretin receptors which causes paralysis of the parasite;
available as a spot on preparation for cats;
effective against GI nematodes, hookworm and A. abstrusus;
absorbed slowly over 2-3 days and thought to be stored in fat;
eliminated slowly in bile and feces

A

Emodepside

(Cyclodepsipeptides)

488
Q

name the small animal anthelmintic

effective against roundworm (adult only);
blocks neuromuscular transmission via GABA-gated chloride channels and causes paralysis of parasite;
rapidly absorbed and metabolized;
wide safety margin, can be used in puppies, kittens and pregnant animals but NOT in animals with liver or renal disease;
should not be used with Pyrantel (agonists)

A

Piperazine

489
Q

name the small animal anthelmintic

diphenylether;
may act by uncoupling oxidative phosphorylation and depleting energy;
given orally to dogs only;
causes neurological signs in cats;
broad spectrum of acticity against GI nematodes and some tapeworms;
irritant and can cause vomiting so give whole tablets to dogs

A

Nitroscante

490
Q

name 4 clinical uses of GnRH

A
  1. induction of follicular growth
  2. induction of ovulation
  3. improvement of conception rates (cattle)
  4. Tx of follicular cysts (dairy cattle)
491
Q

when would you give GnRH in cattle to improve conception rates

A

11-12 days post-service

492
Q

name the 2 categories of gonadotropins

A
  1. pituitary (FSH, LH)
  2. chorionic (CGs)
493
Q

which has a longer half life, FSH/LH or CGs, and why?

A

CGs because more heavily sialylated (more sialic acid residues)

494
Q

name 5 clinical uses of gonadotropins

A
  1. Induction of ovulation
  2. Induction of follicular growth during anestrus
  3. Detection of cryptorchidism (horses)
  4. Induction of spermatogenesis or enhance libido
  5. Induction of superovulation (cattle)
495
Q

what gonadotropin is used to induce ovulation

A

hCG

496
Q

whih gonadotropins are used to induce follicular growth during anestrus

A

eCG / rFSH

497
Q

what gonadotropin stimulation test is used for detection of cryptorchidism in horses

A

hCG

498
Q

which gonadotropins are used to induce spermatogenesis or enhance libido

A

eCG / rFSH

499
Q

when to start rFSH injections for induction of superovulation in cattle

A

mid estrus cycle (day 9-14)

500
Q

name 6 indications for use of oxytocin

A
  1. dystocia due to uterine inertia
  2. promote uterine involution
  3. expulsion of retained fetal membranes (horses)
  4. uterine prolapse
  5. facilitate clearance of uterine discharge (mares)
  6. milk let down
501
Q

name 3 cases where oxytocin is contra-indicated and could lead to uterine rupture if used

A
  1. abnormal fetal position
  2. insufficient cervical dilation
  3. previous uterine surgery
502
Q

name the two blood proteins that bind reproductive steroids

A
  1. sex hormone binding globulin (SHBG)
  2. corticosteroid binding globulin (CBG)
503
Q

what 2 reproductive steroids are bound by sex hormone binding globulin (SHBG)

A
  1. testosterone
  2. estradiol
504
Q

what 2 reproductive steroids are bound by Corticosteroid binding globulin (CBG)

A
  1. cortisol
  2. progesterone
505
Q

what 2 ways do binding proteins regulate reproductive steroid activity

A
  1. regulating steroid metabolism
  2. regulating steroid access to target cells
506
Q

name 2 clinical uses of Progestagens

A
  1. synchroniztion of estrus (cattle)
  2. induction of estrus in anestrus animals
507
Q

name 3 adverse effects of progestagens in small animals

A
  1. uterine disorders (endometrial hyperplasia, pyometra)
  2. adrenal corticol suppression
  3. mammary tumors, pseudopregnancy, exacerbate diabetes
508
Q

what is the main clinical use of PGF2⍺

A

induction of luteolysis

509
Q

name 3 indications of PGF2⍺ as a luteolytic agent in mares

A
  1. persistent CL
  2. termination of pregnancy
  3. synchronization of estrus
510
Q

name 6 indications of PGF2⍺ as a luteolytic agent in cattle

A
  1. luteal cysts
  2. persistent CL
  3. endometritis
  4. pyometra
  5. termination of pregnancy
  6. synchronization of estrus
511
Q

in order to terminate pregnancy, PGF2⍺ must be given before this day of pregnancy in cattle

A

day 150

512
Q

in order to terminate pregnancy, PGF2⍺ must be given before this day of pregnancy in sheep

A

day 50

513
Q

in order to terminate pregnancy, PGF2⍺ must be given before this day of pregnancy in horses

A

day 35

514
Q

what must be present in order for PGF2⍺ to work

A

responsive CL

515
Q

how far apart should 2 injections of PGF2⍺ be given in order to synchronize estrus in cattle

A

11 days

516
Q

name 5 adverse effects of PGF2⍺

A
  1. transient sweating
  2. mild colic
  3. incr. HR
  4. incr. resp. rate
  5. muscle weakness
517
Q

name the hormone

induces Lh/FSH release from the pituitary;
stimulates follicular maturation/ovulation

A

GnRH

518
Q

name the hormone

FSH/LH agonist which stimulates maturation of follicles

A

eCG / PMSG

519
Q

these provide exogenous progesterone source to prevent ovulation (“a CL on a stick”)

A

progesterone implants

520
Q

name the hormone

induces luteolysis

A

PGF2⍺