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Clinical Veterinary Science and One Health 23/24 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Name the factors that influence interspecies PKPD differences.

A

Anatomy
Physiology
Behaviour
Genetics

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2
Q

How does anatomy influence interspecies PKPD differences?

A

Size, skin, muscles, internal organs. Influences administration, absorption and distribution.

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3
Q

How does physiology affect interspecies PKPD differences?

A

Systems like GI, reproductive, liver and kidneys. Impacts on administration, absorption, metabolism and elimination of drugs.

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4
Q

How does behaviour affect interspecies PKPD differences?

A

Impacts on how we administer drugs and impact drugs directly and indirectly.

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5
Q

How does genetics affect interspecies PKPD differences?

A

Explain similarities and differences between and within species. Impact metabolism and affects pharmacodynamics.

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6
Q

What affects the feasibility of the intravenous route?

A

Behaviour and domestication status

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7
Q

What affects the feasibility of the intramuscular route?

A
  • Tolerance – limited in chinchillas, among other species.
  • Behaviour impacts
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8
Q

What complicates the intramuscular route in birds and reptiles?

A

Renal portal system – blood in caudal half of the body drain through the kidneys before going to the heart. So many drugs it is preferable to inject in cranial half

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9
Q

What affects the feasibility of subcutaneous route?

A
  • Variable tolerance
  • Cats – incidence of fibromatous reactions following SC administration of vaccines causing vaccine induced sarcomas
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10
Q

What affects the feasibility of oral route?

A

Feeding behaviours
Mass administrations

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11
Q

What affects the feasibility of intramammary and transdermal routes?

A

Behaviours
Structure of skin
Variation in bioavailability

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12
Q

How does oesophageal anatomy affect interspecies drug absorption and distribution?

A

Cats predisposed to potential retention of tablets, tendency to obstruction/choking in horses

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13
Q

How does the reticulo-rumen affect interspecies drug absorption and distribution?

A
  • Slow emptying at 6-15 hours
  • Keratinised wall = poor absorption, except of weak acids
  • Acidic = trapping of weak bases
  • Dilution and increased residence time of orally administered drugs
  • Microflora of the rumen can inactivate drugs by metabolic or chemical reactions
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14
Q

Describe the plasma concentrations of some oral drugs in ruminants.

A

Sustained plasma concentrations of some drugs after oral administration in ruminants, despite short half lives after IV administration, such as salicylic acid.

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15
Q

How does cellulose binding in herbivores and horses affect drug absorption and distribution?

A
  • Release of the drug with cellulose breakdown
  • Influence of feeding on bioavailability
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16
Q

How does metabolism affect interspecies PK differences?

A

Interspecies quantitative differences in phase I and qualitative differences in phase II metabolism. Cytochrome P450 polymorphisms

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17
Q

How does excretion of drugs differ between species?

A

Urinary pH is determined by diet

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18
Q

What are the factors affecting within species differences?

A

Age
Sex
Disease
Physical state
Mobility
Diet
Genetics
Circadian rhythms

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19
Q

How are medicines responsibly used?

A

Antimicrobial resistance
Anthelmintic resistance
Animal health and welfare
Safeguarding food supply
Food quality and safety
Environmental impact
Public health

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20
Q

How does legislation class different animals?

A

Legislation will say that a pig even if a pet will be classed as a food producing animal. Backyard hen will be treated as a food producing animal as they eat the eggs. Guinea pigs will be treated as a food producing animal in south America. Horses can be taken on and off the food list.

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21
Q

How are distribution categories categorised?

A

By risk

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22
Q

What are POM-Vs?

A

Prescription Only Medicine - Veterinarian. All antibiotics.

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23
Q

What are POM-VPSs?

A

Prescription Only Medicine – Veterinarian, Pharmacist. Most wormers.

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24
Q

What are NFA-VPS?

A

Non-Food Animal – Veterinarian, Pharmacist, SQP

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25
Q

What are AVM-GSLs?

A

Authorised Veterinary Medicine – General Sales List

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26
Q

What are the descending orders of suitability for food producing animals cascade?

A
  1. Medicine authorised in another animal species or for a different condition in the same species.
  2. Human medicine authorised or unauthorised vet medicine for any animal species - must be authorised in food animals.
  3. Medicine prescribed by vet
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27
Q

What are the typical withdrawal periods?

A
  • 7 days for eggs and milk
  • 28 days for meat from poultry and mammals
  • 500 degree days/average water temp ÷ number of days for meat from fish
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28
Q

What are some substances that can be administered to food producing animals?

A

Metronidazole
Griseofulvin
Metoclopramide
Lignocaine
Chlortetracycline – in milk powder
Oestrogens

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29
Q

How can correct dose be administered in food producing animals?

A

55% of visual estimates were within 10% from the reference weight. Underestimating of weight increased with larger animals. Depending on what the medicine is, it may or may not matter. Get farmers to weigh animals, if they can’t, use a weigh tape.

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30
Q

How can safety, animal welfare and product quality be ensured when administering food animal therapeutics?

A
  • Restraint
  • New needle every time
  • Animal welfare – avoid locomotor muscles
  • Carcass/hide damage
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31
Q

What are some particular drugs of health and safety concern?

A

Tilmicosin - if you inject this into yourself, you can kill yourself

PGF2alpha - destroys the corpus luteum if absorbed through skin, if aerosol is a smooth muscle constrictor for asthmatics

Ops - toxicity

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32
Q

Why is prevention better than cure?

A
  • Improved health, productivity and welfare
  • Improved food quality
  • Reduced use of antimicrobial treatments
  • Reduced risk of antimicrobial resistance
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33
Q

How is prevention achieved in food animals?

A
  • Proactive health management
  • Optimising animal husbandry, biosecurity
  • Environment
  • Stocking rate
  • Vaccines
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34
Q

Which medicines must audits be done on?

A

Fluoroquinolones, 3rd and 4th generation cephalosporins, and long acting macrolides

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35
Q

What are the new categories of medicines 2020?

A

Category A - Avoid
Category B - Restrict
Category C - Caution
Category D - Prudence

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36
Q

Describe category A medicines.

A

Includes antibiotics that are currently not authorised in veterinary medicine in the EU.

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37
Q

Describe category B medicines.

A

Refers to quinolones, 3rd- and 4th-generation cephalosporins and polymyxins. (previously called HPCIA)

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38
Q

Describe category C medicines.

A

Covers antibiotics for which alternatives in human medicine generally exist in the EU, but only few alternatives are available in certain veterinary indications.

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39
Q

Describe category D medicines.

A

Includes antibiotics that should be used as first line treatments, whenever possible. These antibiotics can be used in animals in a prudent manner.

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40
Q

What is responsible use of antimicrobials?

A
  • Only if appropriate
  • Right antimicrobial
  • Right dose
  • Complete the course
  • Prophylactically with caution
  • Do not use modern antibiotics (3rd/4th generation Cephalosporins or Fluoroquinolones)
  • Use in accordance with the label
  • Use under the cascade as an exception
  • Use as little as possible and as much as necessary
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41
Q

What are schedule 6 exemption products in terms of drug classification?

A

A way to allow medicines to be used in exotics

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42
Q

How are controlled drugs classified?

A

All CDs are listed in one of five Schedules according to their therapeutic usefulness.

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43
Q

What are schedule 1 CDs?

A

Vets have no authority to possess, such as cocaine.

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44
Q

What are schedule 2 CDs?

A

Ketamine, morphine, pethidine, fentanyl, alfentanil, methadone, the amphetamines, secobarbital.

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45
Q

What are schedule 3 CDs?

A

Buprenorphine, pentobarbital, phenobarbital, midazolam and some minor stimulants, including benzphetamine.

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46
Q

What are schedule 4 CDs?

A

Part I benzodiazepines; part II contains anabolic and androgenic steroids.

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47
Q

What are schedule 5 CDs?

A

Includes preparations of certain CDs (such as codeine, pholcodine, or morphine) which due to their low strength, are exempt from virtually all CD requirements other than retention of invoices for two years.

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48
Q

Which CDs must be kept under safe custody?

A

Schedule 2s except quinalbarbitone
Only exceptions of schedule 3s

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49
Q

Which CDs require extra prescription requirements?

A

Schedule 2 and 3s

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50
Q

What are the prescription validities of CDs?

A

Schedule 2, 3 and 4 = 28 days
Schedule 5 = 6 months

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51
Q

Which CDs require CD register?

A

Schedule 2s

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52
Q

Which CDs require an independent witness for destruction?

A

Schedule 2s

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53
Q

Which CDs have the invoice kept for 2 years?

A

Schedule 2, 3, 4 and 5s

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54
Q

How are CDs recorded?

A
  • Date supplies
  • Name and address of person to whom it was prescribed
  • Name and signature of vet
  • Amount
  • Form of drug
  • Running total (recommended)
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55
Q

If a schedule 2 CD is dispensed to a client, what should also be recorded?

A
  • Name of the person collecting the CD
  • Was proof of identity of the person collecting the drug requested?
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56
Q

Name the 2 major processes of post-authorisation monitoring.

A

Pharmacovigilance
Residue testing

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57
Q

Define suspected adverse reaction.

A

A reaction which is harmful and unintended and which occurs at doses normally used in animals for the prophylaxis, diagnosis or treatment of disease or the modification of physiological function.

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58
Q

What are sympathomimetic and parasympathomimetic drugs?

A

Mimetic drugs activate the effects of the relevant branch of the ANS: directly via post-ganglionic neuron stimulation or indirectly by promoting the effects of neurotransmitters

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59
Q

What are sympatholytic and parasympatholytic drugs?

A

Lytic drugs inhibit the effects of the relevant branch of the ANS: directly by specific receptor blockage leading to inhibition of neuro and humoral stimulation or indirectly by inhibiting neurohumoral transmission.

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60
Q

What type of drug is ephinephrine?

A

Sympathomimetic - acts on alpha and beta adrenoreceptors

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61
Q

What are the effects of epinephrine acting on alpha receptors?

A
  • Vasoconstriction a1 in most areas > increased blood pressure
  • Metabolic effects – decreased insulin and increase in blood glucose, fatty acids, lactic acid and oxygen consumption
  • Splenic contraction a, piloerection, mydriasis, and decrease in intraocular pressure
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62
Q

What are the effects of epinephrine acting on beta receptors?

A
  • Vasodilation B2 in some tissues, such as skeletal muscles, coronary arteries
  • Positive inotropic and chronotropic effects > increased heart rate and stroke volume though can lead to arrhythmias
  • Bronchodilation B2
  • Decreased GI motility B
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63
Q

What are the clinical indications of epinephrine?

A
  • Cardiopulmonary resuscitation
  • Anaphylactic shock
  • Hypotension through less commonly used than noradrenaline
  • Local vasoconstriction, such as prolonged effects of local anaesthesia
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64
Q

What are the unwanted effects of epinephrine?

A
  • Can predispose to arrhythmias and hypertension
  • Care if using adrenaline containing local anaesthetic preparations on extremities
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65
Q

What are the pharmacokinetics of epinephrine?

A

Rapid onset action and very short duration of action, less than 2 minutes.

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66
Q

What type of drug is phenylephrine?

A

Sympathomimetic. Acts on a1 adrenoreceptors

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67
Q

What are the effects of phenylephrine?

A
  • Produces vasoconstriction
  • Increased blood pressure may result in reflex bradycardia
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68
Q

What are the clinical indications of systemic phenylephrine?

A
  • Management of hypotension in small animals and horses
  • Cause splenic contraction in horses with nephrosplenic entrapment
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69
Q

What are the clinical indications of local phenylephrine?

A
  • Management of priapism/penile prolapse in horses – inject into corpus cavenosum
  • Eye drops 2.5% - pupil dilation, ophthalmic exam or surgery, treatment of Horner’s syndrome, part of diagnostic testing for grass sickness in horses.
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70
Q

What are the unwanted effects of phenylephrine?

A

May decrease tissue perfusion and possibly decrease cardiac output

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71
Q

What are the pharmacokinetics of phenylephrine?

A
  • Rapid onset of action
  • Absorbed from mucous membranes
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72
Q

What type of drugs are xylazine, dexmedetomidine and romifidine?

A

Sympathomimetic. Acts primarily on a2 adrenoreceptors, some a1 effects but selectivity varies between drugs

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73
Q

What are the effects of xylazine, dexmedetomidine and romifidine?

A
  • Presynaptic > decreased sympathetic tone > reduced blood pressure
  • Post-synaptic on vascular smooth muscle > vasoconstriction
  • Decreases sympathetic transmission within CNS > sedation and analgesia
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74
Q

What are the clinical indications of xylazine, dexmedetomidine and romifidine?

A
  • Sedation and analgesia in vet species
  • Often referred to as a2 agonists
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75
Q

What type of drug is atipamezole?

A

Sympatholytic

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76
Q

What are the effects of atipamezole?

A
  • Acts as an antagonist a2-adrenoreceptors
  • Reverses/antagonises the effects of the a2-agonists xylazine, (dex)medetomidine and romifidine
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77
Q

What type of drug is dobutamine?

A

Sympathomimetic. B1 effect predominant and selective

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78
Q

What are the B1 effects of dobutamine?

A
  • Positive inotrope > positive chronotrope
  • Minimally arrhythmogenic
  • Effect on BP mainly by increased contractility
  • Dose-dependent, species-dependent
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79
Q

What are the B2 effects of dobutamine?

A

Minimal – limited vasodilation

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80
Q

What are the clinical indications of dobutamine?

A

Treatment of hypotension:

  • In horses during anaesthesia – increases myocardial contractility and cardiac output and promotes muscle perfusion
  • In small animals where cardiac contractility is a concern
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81
Q

What are the unwanted effects of dobutamine?

A

Tachycardia is dose dependent so inject to effect

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82
Q

What are the pharmacokinetics of dobutamine?

A

Rapid onset and short half life (2-3) minutes so administer by infusion

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83
Q

What type of drugs are clenbuterol?

A

Sympathomimetic. Active selectively on B2 receptors

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84
Q

What is the effect of clenbuterol?

A
  • Bronchodilation
  • Tocolytic – produces uterine relaxation in cattle
  • Minimal B1 effect so less cardiac effects
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85
Q

What are the clinical indications of clenbuterol?

A
  • Bronchospasm, management of equine asthma usually in combination with corticosteroids and changes to husbandry (clenbuterol does not reduce inflammation – only produces bronchodilation)
  • Obstetrics - uterine relaxation in cattle
  • Must not be used for any other indication in cattle
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86
Q

What are the unwanted effects of clenbuterol?

A

Sweating, vasodilation leading to hypotension and tachycardia

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87
Q

What are the pharmacokinetics of clenbuterol?

A
  • IV injection in cattle rapidly distributed and excreted
  • Oral administration in horses leads to maximal plasma concentrations in 2 hours and steady state concentrations reached in 3-5 days
  • In horses tolerance develops rapidly if used alone – mitigated by coadministration with corticosteroids
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88
Q

What type of drug is propranolol?

A

Sympatholytic. Non-specific β blockade

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89
Q

What are the effects of propranolol?

A

Mainly cardiac blockade through potential vascular effects

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90
Q

What are the clinical indications of propranolol?

A

Treatment of tachycardia

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91
Q

What are the unwanted effects of propranolol?

A

β1 blockade downside is decreased contractility
β2 blockade produces vasoconstriction and bronchoconstriction

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92
Q

What type of drugs are atenolol and esmolol?

A

Sympatholytic. More specific β1 blockade

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93
Q

What are the effects of atenolol and esmolol?

A

Antagonises the effects of catecholamines to reduce heart rate. Limited β2 blockade means reduced incidence of bronchoconstriction, less vasoconstriction through high doses can result in β2 blockade.

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94
Q

What are the clinical indications of atenolol and esmolol?

A

Treatment of tachycardia, more commonly used than propranolol

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95
Q

What are the unwanted effects of atenolol and esmolol?

A

β1 blockade downside is decreased contractility

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96
Q

What are the pharmacokinetics of atenolol and esmolol?

A

Esmolol IV only – rapid onset of action and rapidly metabolized

Atenolol oral and IV – incompletely absorbed from the GIT and not significantly metabolised

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97
Q

What type of drug is atropine and glycopyrrolate?

A

Parasympatholytic:

  • Atropine is from belladonna plants and glycopyrrolate is synthetic
  • Competitive blockade of muscarinic receptors
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98
Q

What are the effects of atropine and glycopyrrolate?

A
  • Tachycardia and block vagally mediated reflex responses
  • Gastrointestinal smooth muscle relaxation – decreased motility
  • Bronchodilation and decreased secretions
  • Mydriasis
  • Smooth muscle relaxation in urinary tract
  • Decreased sweating (not horses) and decreased salivation
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99
Q

What are the clinical use and pharmacokinetics of systemic IV or IM of atropine and glycopyrrolate?

A
  • Block vagal activity, increase heart rate, treat bradycardia and AV block
  • Onset rapid and duration of action generally short (20-30 minutes)
  • Antispasmodic
  • Treatment of organophosphate toxicity
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100
Q

What are the clinical uses and pharmacokinetics of topical atropine and glycopyrrolate?

A
  • Ocular application as mydriatic. Effective in 15 minutes, peak 2 hrs, residual effects for days
  • Inhalation – treat bronchoconstriction in obstructive syndromes
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101
Q

What are the unwanted effects of atropine and glycopyrrolate?

A
  • Ileus – care in horses and cattle
  • Tachycardia
  • Hypertension when combined with vasopressor
  • Dry mucous membranes
  • Pupillary dilation – avoid exposure to bright sunlight
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102
Q

What type of drug is neostigmine?

A

Parsympathomimetic. Cholinesterase inhibitor

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103
Q

What are the effects of neostigmine?

A
  • Reversible/competitive – neostigmine and edrophonium
  • Irreversible – organophosphate compounds
  • Decrease hydrolysis of Acetylcholine
  • Direct effect on cholinergic receptors
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104
Q

What are the clinical indications of neostigmine?

A

Used in diagnosis of myasthenia gravis

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105
Q

What are the unwanted effects of neostigmine?

A

Bradycardia, salivation, bronchospasm, diarrhoea

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106
Q

What are the pharmacokinetics of neostigmine?

A

Rapid onset of actin within minutes

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107
Q

When are local anaesthetic drugs used?

A
  • Part of a balanced regimen – regional infiltration or epidural in a patient under GA.
  • To provide anaesthesia when in a standing, conscious patient
  • Postoperative pain relief
  • Desensitisation for procedures (cat ET tube)
  • Lameness investigation in horses
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108
Q

What is the difference between epidural and spinal anaesthesia?

A

Epidural – anaesthetics is injected into the epidural space via a catheter

Spinal – the anaesthetic is injected directly into the cerebrospinal fluid via a much smaller needle

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109
Q

What is procaine and its duration?

A

Contain adrenaline. Works via ester linkages, can get allergic reactions due to PABA.

Short acting 50 mins

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110
Q

What is lidocaine and its duration?

A

Rapid onset of 2-5 minutes, short acting 20-40 mins

Lower cardiotoxicity than bupivacaine

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111
Q

What is bupivacaine and its duration?

A

Longer onset than lidocaine, long acting 6 hours

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112
Q

What is mepivacaine and its duration?

A

Horses digital nerve blocks, potency and toxicity greater than lidocaine.

Short acting 2 hours

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113
Q

What is ropivacaine and its duration?

A

Lower CVS and CNS toxicity than bupivacaine.

Long acting 6 hours

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114
Q

What is EMLA and its duration?

A

Topical anaesthesia, rabbit ear IV catherisation

30-45 mins onset of action

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115
Q

What is proparacaine and tetracaine and their duration?

A

Desensitisation of cornea.

Short acting 15 mins in cats and 45 mins in dogs

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116
Q

What increases with potency?

A

Local anaesthetic toxicity

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117
Q

What are the factors of the duration of action of local anaesthetic?

A
  • Penetration/amount of drug reaching the sodium channel – affected by lipid solubility
  • Strength of binding to the channel
  • Speed of removal – dependent on tissue perfusion. Addition of vasoconstrictors, which will increase duration of action
  • Metabolism
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118
Q

How are ester local anaesthetics metabolised?

A

Hydrolysis of the ester link by plasma esterases such as cholinesterases. PABA is formed as a product of hydrolysis and can provoke allergic reactions. The CSF does not contain esterases.

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119
Q

How are amide local anaesthetics metabolised?

A

Broken down by cytochrome P450 enzymes in the liver. Hepatic disease can prolong or limit metabolism. Drugs such as barbiturates that induce enzymes can increase drug breakdown. Drugs that inhibit P450 enzymes (midazolam) can inhibit breakdown.

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120
Q

What formulations does lidocaine come in?

A

Sterile solutions for parental use
Aerosol sprays for nasal/airway use
Topical patches

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121
Q

What are the advantages of making local anaesthetics into a salt solution formulation?

A

LAs are generally poorly water soluble so overcame by salt solution
Lowers the pH so no stinging on injection

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122
Q

Define baricity.

A

The weight of 1 substance compared with the weight of an equal volume of another substance

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123
Q

Why do we not want local anaesthetics to spread high into the epidural space?

A

Could affect the muscles for respiration

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124
Q

How do vasoconstrictors affect local anaesthetics in the body?

A
  • Reduce the speed of systemic absorption and therefore prolong duration of action.
  • Reduces the risk of toxicity
  • Reduces bleeding at the injection site
  • Care with end arterial sites as can get ischaemia
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125
Q

What must a drug be to be systemically active?

A

Must be unbound and unionised

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126
Q

How does plasma protein binding affect local anaesthetic duration?

A

LA which bind more easily to plasma proteins have longer duration of action and lower risk of toxicity

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127
Q

What affects plasma protein binding of local anaesthetics?

A

Lower pH reduces affinity for protein binding and increases risk of toxicity

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128
Q

When is CNS and CVS toxicity seen?

A

CNS toxicity usually seen at lower concentrations that CVS toxicity

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129
Q

How does CNS toxicity present?

A
  • Minor behavioural changes
  • Muscle twitching and tremors
  • Tonic-clonic convulsions
  • CNS depression/respiratory depression and death
130
Q

How is CNS toxicity treated?

A
  • Benzodiazepines (BDZs) to control seizures
  • O2 supplementation
  • Intubation and controlled ventilation if needed
131
Q

How does CVS toxicity present?

A

Hypotension
Dysrhythmias

132
Q

How does CVS toxicity cause hypotension?

A
  • Depression of myocardial contractility
  • Direct relaxation of vascular smooth muscle
  • Loss of vasomotor sympathetic tone
133
Q

How does CVS toxicity cause dysrhythmias?

A
  • Lipophilicity means rapid entry to open sodium channels during systole
  • Drug remains bound to the sodium channel during diastole
  • Presents as re-entrant arrythmias
134
Q

How is CVS toxicity treated?

A
  • Manage bradycardias with an anticholinergic
  • Fluid therapy with inotropic support if needed
  • Intralipid IV may be successful (mop up the LA)
135
Q

How is local anaesthetic toxicity prevented?

A
  • Don’t exceed safe maximum dose
  • If greater volume needed dilute the LA with NaCl 0.9%
  • Use appropriately sized syringes to draw up dose (accuracy)
  • Use appropriately sized needles to minimise tissue trauma
  • Aspirate before injection to confirm you are not in a blood vessel
136
Q

Why are animals premedicated prior to induction of anaesthesia?

A
  • Decrease stress and risk of injury (animal and staff)
  • Balanced anaesthesia – reduced dose of induction agents and reduce dose of maintenance agents
  • Provide analgesia
  • Assists smooth recovery from anaesthesia
  • Reduce side effects of anaesthetic drugs
137
Q

Name the 5 classes of premedication drugs.

A

Phenothiazines
Alpha-2 agonists
Benzodiazepines
Butyrophenones
Opioids

138
Q

Describe the action of phenothiazones.

A

Sedative action, no algesia. Dopamine receptor antagonist in the CNS

139
Q

Describe the action of alpha-2 agonists.

A

Sedative and analgesic action. alpha-2 adrenergic receptor agonist in the CNS

140
Q

Describe the action of benzodiazepines.

A

Sedative action, no analgesia. Enhance the effect of gamma-aminobutyric acid at the GABA receptor

141
Q

Describe the action of butyrophenones.

A

Sedative action, no analgesia. Dopamine receptor antagonist in the CNS, interferes with GABA, norepinephrine and serotonin-mediated neuronal activity

142
Q

Describe the action of opioids.

A

Some species dependent sedation, analgesic effect

143
Q

What are the clinical effects of acepromazine?

A

Sedation and anxiolytic, no analgesia

144
Q

How is acepromazine given as premedication?

A

Widely used for premedication prior to anaesthesia and sedation for procedures. Often used in combination with opioids.

145
Q

What CVS effects does ACP have?

A
  • Peripheral vasodilation
  • Potential to decrease blood pressure – particularly in animals with CVS disease or shock
  • Managed by administration of fluids
146
Q

How does ACP cause anti-arrhythmic action?

A
  • Vasodilation also causes fall in body temperature so is an issue with high body surface to weight ratio
  • Minimal effects of respiration
147
Q

What is the duration of ACP?

A
  • Time to clinical effect after IV administration is 10-15 minutes
  • Clinical effect 30-40 minutes after IM administration
  • Long duration of action (4-6 hours)
148
Q

Describe the pharmacokinetics of ACP.

A
  • Liver metabolised - action more prolonged in animals with liver disease
  • Poor oral bioavailability
149
Q

What are the clinical effects of alpha-2 agonists?

A

Sedation, analgesia and muscle relaxation

150
Q

Why is alpha-2 agonists being potent an advanatge?

A

Significant dose reduction for anaesthetic induction and maintenance

151
Q

What is the reversal agent for alpha-2 agonists?

A

Atipamezole

152
Q

What are the CVS effects of alpha-2 agonists?

A

Bradycardia, reduced CO, second degree AV block. BP rises initially then falls either back to normal or hypotensive.

153
Q

What are the respiratory effects of alpha-2 agonists?

A

Variable between species and individuals within a species – respiratory depression can be seen in some but not all patients. Rate decrease with no overall effect on minute volume or blood gases.

154
Q

What are the GI effects of alpha-2 agonists?

A

Emetic in dogs and cats
Can depress GI activity
Bloat in ruminants
Stasis in dogs
Reduced insulin secretion/transient hyperglycaemia

155
Q

What are the renal and uterine effects of alpha-2 agonists?

A

Increase urine production by a decrease in secretion of vasopressin

Uterine contractility – depend on dose and concentrations of oestrogen and progesterone therefore avoid in near term animals due to the risk of abortion

156
Q

Describe the duration of alpha-2 agonists.

A
  • Rapid clinical effect after IV administration - 5 minutes
  • Peak effects at 30 minutes
  • Clinical effect 15 minutes after IM administration
  • Often reversed with atipamezole, if not duration of action 2-3 hours
157
Q

How are alpha-2 agonists metabolised?

A

Hepatic metabolism – action more prolonged in animals with liver disease

158
Q

What are the clinical effects of benzodiazepines?

A

Minor tranquilisers, muscle relaxation, anticonvulsant

159
Q

Describe the sedative effect of benzodiazepines.

A

Unreliable in healthy animals and can cause excitement. Good sedation in sick or young animals. Combine with an opioid, ketamine or a2 agonists to improve sedation. Often used as adjuncts to anaesthetic induction agents for co-induction

160
Q

Why are benzodiazepines a good choice for unhealthy patients?

A

As they have minimal effects on CVS and respiratory system

161
Q

What is the effect of benzodiazepines on the musculoskeletal system?

A

Potentiates GABAergic mediated muscle relaxation of inhibitory neurones at the level of the spinal cord. Often administered with drugs that do not provide muscle relaxation – such as ketamine

162
Q

What is the benzodiazepine reversal agent?

A

Flumazenil

163
Q

What are the clinical effects of butyrophenones/fentanyl?

A
  • Alone provides surgical anaesthesia for minor surgery or diagnostic techniques
  • Duration of sedation/immobilisation 30-60 minutes
  • Poor muscle relaxation when administered alone – good with the addition of midazolam
  • If administered with midazolam/diazepam, good surgical anaesthesia with muscle relaxation for 20-40 minutes
164
Q

How can the respiratory depression caused fentanyl be reversed?

A

Administration of naloxone/butorphanol/buprenorphine

165
Q

How should you care for the premedicated patient?

A
  • Quiet environment
  • Need to be observed regularly/continuously
  • Think ABC/airway, breathing and circulation)
  • Monitor temperature, pulse, respiration, mucous membranes
  • Ideally use a pulse oximeter
  • Ideally record observations
166
Q

What could go wrong with premedication?

A
  • Excitement/excessive sedation
  • Airway obstruction (vomit, anatomical)
  • CVS effects up to and including cardiac arrest
  • Patient can’t compensate for existing condition/hidden condition exposed
  • Something odd develops
167
Q

How can injectable anaesthetic agents be used for intramuscular anaesthetic protocols?

A

Combine the sedation/premedication and induction phase. So in triple/quad anaesthetics (cats), an opioid, an alpha-2 agonist, ketamine and with/without a benzodiazepine. Combined in same syringe and administer it intramuscularly. Produces induction of anaesthesia and unconsciousness.

168
Q

List the injectable anaesthetic agents.

A
  • Propofol – dogs, cats
  • Alfaxalone – dogs, cats, rabbits
  • Ketamine – horses, dogs, cats
  • Tiletamine/zolazepam – dogs, cats
169
Q

Which of the injectable anaesthetic agents are GABA agonists?

A

Propofol
Alfaxalone
Barbiturates
Zolazepam

170
Q

Which of the injectable anaesthetic agents are NMDA antagonists?

A

Ketamine
Tiletamine portion of tiletamine/zolazepam

171
Q

Name 2 drugs used for euthanasia.

A

Pentobarbital

Secobarbital Sodium (quinalbarbital sodium) + Cincocaine Hydrochloride = Somulose

172
Q

How does somulose cause euthanasia?

A

The barbiturate acts to enhance to GABA actions, local anaesthetic acts to block sodium channels and within the heart will cause blockade to interrupt the cardiac action.

173
Q

List the factors affecting the effects of drugs.

A

Blood flow to the brain
Amount of non-ionized drug
Lipid solubility
Molecular size
Concentration gradient
Protein binding
Distribution
Metabolism
Excretion

174
Q

What are the features of the ideal injectable anaesthetic agent?

A
  • Rapid onset – one “arm to brain” time
  • Non-irritant
  • Minimal cardiopulmonary effects
  • Rapidly metabolised and eliminated
  • Non-cumulative
  • Good analgesia
  • Good muscle relaxation
175
Q

Describe the properties of propofol.

A
  • GABA agonist
  • Rapid onset of action
  • Highly plasma protein bound
  • Lipid soluble
  • Rapidly metabolised and eliminated
  • Non-cumulative in dogs and not cats
176
Q

What are the physiological effects of propofol?

A
  • Post-induction apnoea
  • Hypotension – myocardial depression and peripheral vasodilation
  • No analgesia but has fair muscle relaxation
  • Prolonged use = RBC damage = Heinz body anaemia in cats
177
Q

What are the properties of alfaxalone?

A
  • High therapeutic index
  • Non-irritant if perivascularly
  • 20% plasma protein bound
  • Rapid onset
  • Rapid metabolism and elimination
  • Non-cumulative
178
Q

What are the physiological effects of alfaxalone?

A
  • Some respiratory depression
  • Preserves baroreceptor tone – HR increases in response to reduced BP
179
Q

What are the properties of ketamine?

A
  • Poor muscle relaxation – not used as sole agent
  • Reflexes maintained
  • Analgesia/antihyperalgesia
  • Slow onset
  • Non-cumulative through active metabolite nor-ketamine
  • 50% plasma protein bound
180
Q

What are the physiological effects of ketamine?

A
  • Poor muscle relaxation – not used as sole agent
  • Reflexes maintained
  • Sympathetic stimulation
  • Maintains CV (via adrenaline release) and respiratory function
181
Q

How is ketamine metabolised and excreted?

A

Metabolised by the liver and active metabolite nor-ketamine must be excreted via the kidneys so this can be compromised in animals with renal dysfunction.

182
Q

What are the properties of tiletamine/zolezepam?

A
  • IM or IV
  • Repeated dosing = poor recovery
  • Difference in PK in dogs and cats – zolazepam is metabolised quicker than tiletamine in dogs, leading to poor quality, excitable recoveries
183
Q

What are the properties of thiopental?

A
  • Powder made up to 2.5-5%
  • Alkaline
  • Perivascular tissue necrosis – secure IV access
  • Rapid onset
  • High plasma protein bound 80%
184
Q

What are the physiological effects of thiopental?

A
  • Prolonged recovery in sighthounds
  • Moderate cardiorespiratory depression – ventricular bigeminy
185
Q

List the factors affecting the recovery from injectable anaesthetics?

A
  • Drug factors including dose
  • Species, breed and age
  • Co-morbidities
  • Cardiovascular function
  • Hepatic function
  • Renal function
  • Hypothermia
  • Concurrent drug administration
186
Q

When may TIVA be useful?

A

To reduce exposure to inhalant anaesthetic agents, in the field or under specific conditions

187
Q

What are the ideal properties of TIVA?

A
  • Rapid metabolism and elimination
  • Fast onset
  • High therapeutic index
  • Pharmacokinetics available
188
Q

What characteristics of an anaesthetic drug molecule facilitates the most rapid onset of action?

A

Non-ionised, small molecule, low plasma protein binding

189
Q

Which injectable anaesthetic agent would be the most affected by hypoalbuminaemia?

A

Propofol as 98% plasma protein bound. If there is significant hypoalbuminaemia then, if a fixed dose is administered, a greater proportion of it will be the unbound fraction compared to an animal with normal serum albumin. The free/unbound fraction crosses the cell membranes to the effect site, onset will be faster due to larger concentration gradient. There is potential for overdose.

190
Q

Which intravenous anaesthetic agent would be the most suitable for administration by CRI for maintenance for anaesthesia in cats?

A

Alfaxalone is non-cumulative in cats so can be administered by infusion for anaesthetic maintenance. Recovery from anaesthetic will be relatively rapid. While propofol can be administered by infusion in cats, they lack he glucuronidation pathway for metabolism of the drug so it is cumulative. Recovery can be prolonged, which can be problematic after routine anaesthesia if a propofol is desirable.

191
Q

Which injectable anaesthetic agent causes necrosis if accidentally injected perivascularly? How would you mitigate this risk?

A

Thiopental. Place an intravenous catheter and check its patency and placement before injecting thiopental.

192
Q

What steps can you take to minimise the dose required and therefore adverse effects in dogs, cats and rabbits?

A
  • Most healthy cats and dogs, ACP/(dex)medetomidine + opioid will significantly reduce the dose of injectable anaesthetic required.
  • In rabbits (dex)medetomidine + opioid will reduce the dose required.
  • In sick animals administration of ACP or dexmedetomidine may not be appropriate so +/- benzodiazepine
193
Q

Hypotension can occur after administration of propofol or alfaxalone. What animals will be at most risk of developing significant hypotension and how would you mitigate this risk?

A

Animals in shock. They are at risk of developing significant hypotension during induction. Hypovolaemia should be corrected as much as possible before proceeding with anaesthesia with IVFT. The underlying cause of shock/hypovolaemia should be identified to help with anaesthetic planning – CVS dysfunction, haemorrhage.

194
Q

In secondary haemostasis, what protein becomes cross-linked to form a scaffold for the clot?

195
Q

Which are the Vitamin K dependent clotting factors?

A

II, VII, IX, X

196
Q

What is the vascular response of primary haemostasis?

A

Vasoconstriction and exposure of subendothelial collagen, fibronectin, von Willebrand’s factor, tissue factor

197
Q

What is the platelet response of primary haemostasis?

A

Adhere via pseudopodia then via vWF, glycoprotein receptors and fibrinogen. Activated platelets produce chemotactic granules causing further platelet aggregation and also expose phospholipid (PF3) causing trigger coagulation cascade.

198
Q

What is vitamin K?

A

A fat-soluble vitamin, requires solubilisation by bile acids for absorption. Aids in production of clotting factors II, VII, IX and X

199
Q

What is vitamin K used commonly to treat?

A

Coumarin-based rodenticide intoxication

200
Q

What is vitamin K used less commonly to treat?

A

Poor coagulation due to lack of absorption of vitamin K because severe biliary obstruction, or severe gastrointestinal disease

201
Q

Distinguish first and second generation vitamin K antagonists.

A

1st – warfarin, dicoumarin. Less potent, variable half-life

2nd – brodifacoum, bromadiolone, difenacoum. Highly potent, long half-life

202
Q

How is vitamin K1/phytomenadione administered?

A

S/C then orally with fatty meal
Not I/V = anaphylaxis
Not I/M = bleeding

203
Q

How should vitamin K1/phytomenadione be used as a treatment?

A
  • 7-28 days depending on toxin
  • Prothrombin time (PT) should normalise within 12-24 hours
  • Check PT 2 days after finishing treatment and continue if necessary
204
Q

Why should vitamin K3 be avoided?

A

Poor efficacy, side effects

205
Q

When are topical haemostatic drugs used?

A
  • Assist in control of persistent capillary bleeding
  • Ideally provide good haemostasis, minimal tissue reactivity, easy to sterilise and handle
  • Only work if no haemostatic or fibrinolytic defects
206
Q

How are epinephrine and norepinephrine a haemostatic drug?

A

Immediate transitory vasoconstriction. May help with local control of small vessel bleeding

207
Q

How do silver nitrate and ferric salts act as haemostatic drugs?

A

Precipitate proteins and seal off blood vessels. Only used superficially

208
Q

What are some examples of haemostatic sponges and how they are used as haemostatic drugs?

A

Cellulose, gelfoam/gelatin. Act mainly as a scaffold. Used in theatre for surgical ooze.

209
Q

How are thrombogenic coils used as haemostatic drugs?

A

Thrombogenic fibres that induce fibrosis. Used to treat PDA/persistent ductus arteriosus.

210
Q

What is ddAVP?

A
  • Desmopressin acetate
  • Synthetic analogue of vasopressin/ADH
211
Q

What is ddAVP used to treat?

A

Increase levels of vWF in dogs with vWD e.g. to facilitate surgery
Central diabetes insipidus but very rarely

212
Q

What is tranexamic acid?

A

Injectable and oral preparations. Synthetic lysine analogue that reversibly binds to plasminogen, meaning plasmin can’t act on fibrin, which reduces bleeding

213
Q

What is tranexamic acid used to treat?

A

Has been used as adjunct treatment for dogs with angiostrongylosis, splenic haemangiosarcoma, and trauma

214
Q

What are the side effects of tranexamic acid?

A

Mainly GI, dose dependent, retinal changes with high dose prolonged treatment

215
Q

What is aspirin?

A

An NSAID that, uniquely, causes irreversible inhibition of platelet cyclo-oxygenase

216
Q

What does aspirin cause?

A

Reduced production of eicosanoids required for haemostasis, leading to reduced platelet aggregation. At lower doses has anti-platelet effects

217
Q

What is clopidogrel?

A

A prodrug that needs to be activated so onset of action slow

218
Q

How does clopidogrel cause reduced platelet aggregation?

A

Inhibition of platelet ADP receptors, which prevents activation of glycoprotein IIb/IIIa receptor needed for platelet aggregation

219
Q

What is clopidogrel used to treat?

A

Used to reduce risk of thrombi in cats with significant heart disease

220
Q

What are the indications for immunosuppression?

A

Immune mediated haemolytic anaemia
Immune mediated thrombocytopenia
Immune mediated polyarthritis
Steroid responsive meningitis arteritis
Inflammatory bowel disease
Glomerulonephritis

221
Q

Which drugs can be immunosuppressive at higher doses?

A

Glucocorticoids

222
Q

What are the immunological effects of glucocorticoids?

A
  • Non-genomic effects
  • Increased expression of anti-inflammatory proteins
  • Decreased expression of pro-inflammatory proteins
223
Q

Rank the glucocorticoids from lowest to highest anti-inflammatory potency.

A

Hydrocortisone
Prednisolone
Dexamethasone

224
Q

Describe short acting glucocorticoids.

A

Sodium phosphate and sodium succinate esters. Very soluble, attain serum level quickly, metabolised rapidly

225
Q

Describe the long acting glucocorticoids.

A

Acetate or diacetate esters. Poorly water soluble, absorbed and metabolised more slowly

226
Q

What are the effects of topical glucocorticoids?

A

Less systemic side effects. However, systemic absorption and side effects can occur.

227
Q

List the side effects of glucocorticoids.

A
  • Pot-bellied (steroid hepatopathy)
  • Polyphagic
  • Panting
  • PUPD
  • Hair coat changes
  • Delayed wound healing and infections
  • Muscle wasting, exercise intolerance
  • Soft tissue mineralisation
  • GI ulceration
  • Insulin resistance (diabetes mellitus)
  • Increased ALKP on blood tests (dogs)
  • Hyperadrenocorticism
228
Q

What does long term glucocorticoid use cause?

A

Suppression of hypothalamic-pituitary-adrenal axis and adrenal atrophy, leading to Addisonian crisis. Remember to taper dose before stopping treatment.

229
Q

Which patients should glucocorticoids not be used in?

A
  • On NSAIDS – GI ulceration risk
  • With pre-existing corneal ulcers
  • Pregnant (abortion)
  • Infectious disease
230
Q

Name 5 adjunctive immunosupressants.

A

Ciclosporin
Azathioprine
Chlorambucil
Mycophenolate mofetil
Leflunomide

231
Q

What does ciclosporin cause?

A
  • Results in reduced IL-2
  • Metabolism occurs via P450
232
Q

What are the side effects of ciclosporin?

A

Acute GI signs (most common)
Gingival hyperplasia
Hirsutism
Secondary infections

233
Q

What is ciclosporin used for?

A

Eye ointment used for keratoconjunctivitis sicca

234
Q

What is the effect of azathioprine?

A
  • Inhibits purine synthesis
  • Metabolism occurs via thiopurine methyltransferase
235
Q

What are the adverse effects of azathioprine?

A

Myelosuppression
Hepatotoxicity
GI signs
Pancreatitis

Do not use in cats

236
Q

What is chlorambucil?

A

Alkylating agent with a slow onset of action

237
Q

What are the adverse effects of chlorambucil?

A

Myelosuppression and GI side effects

238
Q

How does Mycophenolate mofetil work?

A

Inhibits purine synthesis
Rapid onset

239
Q

What are the side effects of mycophenolate mofetil

A

Less likely to cause side effects, mainly causes GI side effects

240
Q

What are the effects of leflunomide?

A
  • Inhibits pyrimidine synthesis
  • Less likely to cause side effects
241
Q

What side effect is most likely with drugs acting on the cell cycle?

A

Bone marrow depression

242
Q

Myelosuppression will reduce cell counts for cells with the shortest lifespan first. Rank platelets, red cells and neutrophils from shortest to longest lifespan.

A

Neutrophils
Platelet
RBC

243
Q

How is parapoxvirus an immunopotentiating drug?

A

Inactivated strain available as licenced product for horses for infections or stress induced disease, like EHV. Thought to induce interferon-gamma production by lymphocytes. Non-specific immune stimulation begins few hours-days and lasts 10-14 days

244
Q

Describe the action of domperidone as a immunopotentiating drug.

A

Dopamine antagonist – prokinetic, antiemetic and increases prolactin. Prolactin biases the immune response in favour of cell-mediated (TH1) type response. Leishmania treatment

245
Q

What is an alternative method of delivering steroids long term?

246
Q

Which immunosuppressive treatment is contraindicated when a dog is receiving NSAIDs (given the increased risk of GI ulceration)?

A

Prednisolone

247
Q

What are the properties of the ideal inhalational agent?

A
  • Non-irritant
  • Minimal effects on cardiovascular and respiratory function
  • Rapid uptake and elimination
  • Non-toxic
  • Non-flammable and chemically stable
  • Easily vaporised
  • Good analgesia and muscle relaxation
248
Q

What is MAC?

A

Minimum alveolar concentration - concentration required to prevent purposeful movement on response to a supramaximal noxious stimulus in 50% of subjects

249
Q

How can MAC be reduced?

A

Drugs such as pre-med, hypothermia, pregnancy, geriatric and neonatal animal and hypothyroidism

250
Q

How can MAC be increased?

A

Hyperthermia, young animals, hyperthyroidism, administration of catecholamines and sympathomimetics

251
Q

What administrational properties of inhalation agents result in faster uptake and recovery?

A
  • Higher concentration of inspired air
  • Good alveolar ventilation
  • Lower blood gas solubility
  • Lower cardiac output
252
Q

What affects the distribution of inhalational agents?

A

Blood tissue solubility. Lower solubility = rapid onset of action

253
Q

How does isoflurane meet the criteria for ideal anaesthetic agent?

A
  • Can be irritant to mucous membranes
  • Dose dependent cardiorespiratory depression
  • Rapid uptake and elimination via lungs, less than 1% biotransformation by liver, solubility coefficient 1.4
  • Non-toxic
  • Non-flammable and chemically stable
  • Easily vaporised
  • No analgesia
254
Q

How does sevoflurane meet the criteria for ideal anaesthetic agent?

A
  • Better tolerated than isoflurane
  • Dose dependent cardiorespiratory depression
  • Rapid uptake and elimination via lungs, 3% biotransformation by liver, solubility coefficient 0.69 (faster than isoflurane)
  • Non-toxic
  • Non-flammable and chemically stable, can produce compound A with soda lime
  • Easily vaporised
  • No analgesia
255
Q

Which inhalational anaesthetic is a gas at room temperature and sea level?

A

Nitrous oxide

256
Q

What combination of factors would lead to the fastest onset of anaesthesia with an inhalational agent?

A

High inspired concentration, low cardiac output and high alveolar ventilation

257
Q

Why does sevoflurane produce a more rapid onset of anaesthesia than isoflurane?

A

It has a lower blood gas solubility coefficient

258
Q

Which inhalational agents have UK marketing authorisation for administration to cats?

A

Isoflurane and sevoflurane

259
Q

Compound A is produced by a reaction of which anaesthetic agent with soda lime?

A

Sevoflurane

260
Q

What are the risk factors of equine anaesthesia and sedation?

A
  • Age
  • Duration of anaesthesia – directly related to outcome in horses, want it to be under 2 hours
  • Time of surgery
  • Operation type
261
Q

Which drugs are used for equine anaesthesia?

A
  1. Acepromazine
  2. α2-agonist sedation
  3. Wait 5 minutes
  4. Induction – ketamine or diazepam, thiopental, or GGE
262
Q

What is GGE?

A

Guaiphenesin - centrally acting muscle relaxant. No analgesic. IV only, tissue damage if perivascular

263
Q

What analgesics are used in horses?

A
  • NSAIDs – before anaesthesia if possible, horses less predisposed to renal effects so given even if hypotensive horses
  • Opioids
  • α2-agonists
  • Ketamine
  • Local anaesthetics
264
Q

During equine anaesthesia, when should ET tube be removed?

A

When respiratory effort increases

265
Q

What is equine post anaesthetic myopathy?

A
  • Damage to muscles during anaesthesia, thought to be related to BP
  • Lame to unable to stand
  • Muscles hard, swollen and painful on palpation
  • Myoglobinuria
  • Elevated muscle enzymes
266
Q

What is the risk of acepromazine in horses?

A

Risk in breeding stallions, damage to penis, caution in castrated stallion, make sure you have consent

267
Q

What is the risk of the opioid pethidine in horses?

A

Spasmodic pain and colic but causes pain/stinging upon injection

268
Q

Which alpha-2 agonists can be used in horses?

A

Xylazine
Detomidine
Romifidine

269
Q

Which opioids can be used in horses?

A

Butorphanol
Buprenorphine
Pethidine
Morphine
Methadone

270
Q

Which sedatives are used in cattle?

A

Xylazine IM, care taken in the 1st month of pregnancy, contraindicated for use at latter stages of pregnancy except parturition

Detomidine IM or IV, do not use in last trimester of pregnancy

271
Q

Which sedatives are used in pigs?

A

Azaperone IM

272
Q

Which sedatives are used in sheep?

A

None licensed

273
Q

Why is situational awareness important for farm animal sedation and anaesthesia?

A

Risk of recumbency and paradoxical aggression

274
Q

How is farm animal sedation and anaesthesia different to small animal?

A
  • Rumenal tympany and regurgitation and subsequent aspiration potential
  • High likelihood of pregnancy affects drug selection
  • Atipamezole not routinely used
  • Not given with opioids
275
Q

How is cattle sedation and anaesthesia different to horses?

A

Dose of xylazine 10 x less in cattle than horses

276
Q

How is pig sedation and anaesthesia different to small animal?

A

Pigs are very resistant to the sedative effects of alpha-2-adrenoreceptor agonists so very high doses needed

277
Q

What happens when xylazine is used in sheep?

A

Pulmonary oedema

278
Q

What is the only local anaesthetic used in cattle?

A

Procaine Hydrochloride + epinephrine bitartrate

Care with extremities due to vasoconstriction. Not IV, intra-articular or epidural

279
Q

What sort of productive drugs are used in large animal veterinary practice?

A
  • Synchronisation and stimulation of oestrous and ovulation – GnRH analogues, gonadotropins, prostaglandins, progestins
  • Pregnancy termination/induction of parturition – prostaglandins, corticosteroids
  • Adjunctive treatment for endometritis – prostaglandins, antibiotics
  • Problems at parturition – oxytocin, clenbuterol (a beta-2 agonist used to relax the uterus)
280
Q

What are the sort of productive drugs used in small animal veterinary practice?

A
  • Oestrous suppression in bitches – progestins
  • Pregnancy termination/treatment of pyometra – progesterone antagonist
  • False pregnancy – prolactin inhibitor, progestin
  • Problems at parturition – oxytocin
  • Chemical castration – GnRH analogue
281
Q

What is the half life of GnRH and analogues?

A

2-4 minutes

Injectable analogues have a peak activity an hour post injection

282
Q

Describe the release of GnRH.

A

Episodic and pulsatile

283
Q

What are the main uses of GnRH analogues?

A
  • Treat infertility by stimulating FSH/LH production to induce ovulation at time of breeding in horses and cows and inducing oestrous in dogs and cats
  • Treat cystic ovaries in cows
  • Oestrous synchronisation for AI or embryo transfer with PGF2a and in some protocols progestins in cattle
  • Terminating oestrous in ferrets and cats
284
Q

If GnRH analogues are given as long acting analogues, what is this counteractively lead to?

A
  • Down-regulation of GnRH receptors on pituitary gonadotrophic cells
  • Reduced production of gonadotrophins – medical castration Deslorelin used in dogs and ferrets as an implant
285
Q

What is the effect of LH and FSH on males?

A

LH causes Leydig cells to produce testosterone. FSH causes Sertoli cells to produce proteins and nutrients for sperm.

286
Q

What is the effect of LH and FSH on females?

A

FSH/LH causes ovarian follicular development and induction of ovulation. LH causes corpus luteum to develop after ovulation.

287
Q

What is hGC and its effect?

A

Human chorionic gonadotropin – produced only in primates from placental cells. Acts like LH and causes follicle maturation, induction of ovulation and development of the CL.

288
Q

What is eCG/PMSG and its effect?

A

Equine CG/pregnant mare serum gonadotropin/PMSG – produced from endometrial cups of early pregnant mares to induce secondary corpora lutea, maintaining primary CL and progesterone secretion. FSH like but also has LH like activity, enough to induce ovulation.

289
Q

What are the side effects of gonadotropins?

A

Have the side effects of anaphylaxis and antibody production

290
Q

What are the clinical uses of hCG and eCG?

A
  • Treatment of infertility
  • Cows – cystic ovaries, superovulation
  • Induce and synchronise oestrus
  • Males – reduced libido
291
Q

What is oxytocin release stimulated by?

A

Stimulated via sensory nerves in vagina, cervix and suckling reflex

292
Q

What is the function of oxytocin?

A

Uterus stimulates frequency and force of smooth muscle contractions, mammary gland milk ejection

293
Q

What are the clinical uses of oxytocin?

A
  • Induction of labour in many species – need a fully dilated cervix, do not use in obstructive dystocias
  • Milk let down – bitch, cow with mastitis to facilitate stripping, heifers in parlour
  • Adrenaline reduces the effect
294
Q

What are the side effects of oxytocin?

A

Repeated/high doses may lead to painful contractions and rarely uterine rupture. Avoid accidental self-injection

295
Q

What is the effect of prostaglandin analogues?

A

Luteolytic - luteolysis and reduction in progesterone production

296
Q

What are the side effects of prostaglandin analogues in animals?

A
  • Increased smooth muscle tone leads to diarrhoea, abdominal pain, brocnhocontriction, increased blood pressure
  • Increased risk of retained placenta
  • Only give IM
297
Q

What are the side effects of prostaglandin analogues in people?

A
  • Accidental self-injection or absorption across the skin
  • Abortion and bronchoconstriction
298
Q

What are the clinical uses of prostaglandin analogues?

A
  • Oestrus synchronisation in cows
  • Sub-oestrus/silent heat in cows and horses
  • Cystic ovarian disease in cows
  • Induction of abortion in cows and horses
  • Induction of parturition in cows and pigs, parturition 3 days later
  • Treatment of endometritis in cows)/pyometra in bitches – not recommended in bitches
299
Q

What is the pharmacokinetics of progestins?

A

Rapidly metabolised in liver with very low bioavailability and short half-life

300
Q

What is the effect of progestins?

A

Negative feedback on GnRH and FSH/LH suppresses oestrous and ovulation

301
Q

What are the side effects of progestins in people?

A

Pregnant women or anyone with progesterone-dependent tumours or thrombo-embolic disorders shouldn’t handle products

302
Q

How are progestins administered in large animals?

A

Intravaginal devices – PRID/CIDR in cows with progesterone, chronogest in sheep with flugestone

303
Q

What are the uses of large animal intravaginal administration of progestins?

A
  • In cycling animals to synchronise oestrous for groups of animals or for donor/recipient for embryo transfer
  • In non-cycling animals to induce and synchronise oestrous
  • In the treatment of cystic ovarian disease in cattle
304
Q

What is the effect of oral administration of progestins in horses?

A

Suppression of oestrous in mares with significant follicular activity. Control of timing at start of oestrous and synchronisation of ovulation

305
Q

What is the effect of oral administration of progestins in pigs?

A

Synchronisation of oestrous

306
Q

What are the uses of progestins in small animals?

A
  • Oestrous control
  • False pregnancy – once only
  • Feline military dermatitis (flea allergy)
307
Q

What are the side effects of progestins in small animals?

A
  • Risk of pyometra, especially if previously received other progesterone products)
  • Risk of diabetes mellitus as they antagonise the actions of insulin
  • Mammary hypertrophy
  • Adrenal suppression
  • Local skin changes
308
Q

What is the effect of progestins in male small animals?

A

Effects of testosterone through a variety of mechanisms:
- Prevents binding of androgens to prostatic receptors
- Blocks transport of testosterone into prostate

309
Q

What is progestin used to treat in male dogs?

A

Benign prostatic hypertrophy in dogs

310
Q

What is estriol?

A

An oestrogen-based drug

311
Q

What is estriol used to treat?

A

Used in spayed bitches to treat hormone-dependent urinary incontinence

312
Q

What are the adverse reactions of estriol?

A

Swollen vulva, swollen mammary glands, attractiveness to male seen in 5-9% of bitches at high end of dose range. Reversible if dose lowered

313
Q

What is aglepristine?

A

Injectable progesterone-antagonist

314
Q

What is aglepristine used for?

A
  • Pregnancy termination in bitches (up to 45 days post mating) and queens (up to 35 days post-mating)
  • Medical management of pyometra in bitch (recurrence common; surgery advised)
  • Progesterone-induced acromegaly in dogs and fibroadenomatous mammary hyperplasia in cats
315
Q

What are the side effects of aglepristine?

A
  • Transient pain at injection site
  • Warn owner of possible early return to oestrus post abortion
  • Abortion may be partial
  • Anti-glucocorticoid activity
  • Self injection causes significant local reaction
316
Q

What is cabergoline?

A

Prolactin inhibitor

317
Q

What is cabergoline used for?

A

Used to treat false pregnancy in bitches. Behavioural signs resolve first, then reduction in mammary gland size, then finally suppression of lactation

318
Q

What are the side effects of cabergoline?

A
  • Vomiting
  • Anorexia
  • Do not use in pregnant animals – may cause abortion
  • Hypotension (don’t use under GA)
319
Q

What is nandrolone?

A

Anabolic steroid – testosterone-derivative

320
Q

What is nandrolone used for?

A

Some forms of aplastic anaemia and to counteract catabolic states

321
Q

What are the side effects of nandrolone?

A
  • Do not use in pregnant animals
  • May cause strong urine odour in cats
  • Caution in patients with liver disease
322
Q

What is melatonin used for?

A

For early breeding. 30 weeks prior to intended start of lambing, remove ewes from sight/sound/smell of rams/billies

Clinical Veterinary Science and One Health 23/24 (36 decks)

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