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Year 2 NSF > Central Nervous System Pharmacology > Flashcards

Central Nervous System Pharmacology Flashcards

1
Q

What is the difference between a sedative given at a low dose and high dose?

A

Low dose causes animal to be calm and drowsy

High dose causes sleep but not anaesthesia

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2
Q

What does a low and high dose of a tranquilliser cause?

A

Low- calm but alert and responsive

High- Catalepsy (altered state of consciousness, not asleep)

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3
Q

What does an anxiolytic cause?

A

Calm with altered response to stimuli

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4
Q

What is a neuroleptic?

A

Specifically the effects of phenothiazines or butyrophenones in the CNS

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5
Q

What is neuroleptanalgeisa?

A

Combination og neuroleptic and an opioid

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6
Q

What are the 4 main classes of sedatives?

A

Alpha 2 agonists- most common
Phenothiazines
Butyrophenones
Benzodiazepines- least common

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7
Q

What is the term for sedatives that effect post synaptic receptors and pre-synaptic receptors?

A

Post- Symptathomimesis

Pre- Sympatholysis

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8
Q

What is the mechanism of action of alpha 2 agonists?

A

Endogenous neurotransmitter that binds to alpha 2 is noradrenaline
Exogenous a2 is designed to be variously selective fat a2 receptors
Most a2 receptors in periphery are post synaptic so peripheral effects mainly sympathomimetic- vasodilation
Most a2 receptors are pre synaptic so sympatholytic- sedation

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9
Q

What is the mechanism of action of phenothiazines?

A

Only ace-romaine licensed
Antagonists
Antagonist at receptors alpha 1 adreno-receptors (vasodilation) , dopamine 2 receptors (sedation, muscle relaxation), histamine receptors (anti-emetic, reduces hypersensitivity), serotonin receptors (decreased alertness), muscarinic (reduced parasympathetic tone)
In order of most effected to least

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10
Q

What is the mechanism of action of butyrophenones?

A

Similar to phenothiazines
Dopamine receptor 2 agonists- sedation and muscle relaxation
Histamine receptor antagonists- anti-emetic, reduces hypersensitivity

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11
Q

What is the mode of action of benzodiazepines?

A

Endogenous neurotransmitter that binds to GABA receptors- an inhibitory neurotransmitter
Causes decreases resting membrane potential

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12
Q

How are alpha 2 agonists administered?

A

Water soluble so can be injected intravenously and intramuscularly
Molecules are lipid soluble so can be subcutaneous or epidurally or orally

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13
Q

How are phenothiazines administered?

A

Water soluble so IV and IM
Lipid soluble so SC, orally
Tablets least effective

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14
Q

How are butyrophenones administered?

A

Intraperitoneal and IM

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15
Q

How are benzodiazepines administered?

A

IM and IV

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16
Q

What are examples of a2 agonists in order of increasing length?

A 
Xylazine 
Detomidine
Romfidine
Medetoidine
Dexmedetomidine
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17
Q

What is an example of a Phenothiazines?

A

Acepromazine

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18
Q

What is an example of a butyrophenones

A

Fluanisone

Azeperone

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19
Q

What is an example of a benzodiazepines?

A

Diazepam and midazolam

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20
Q

What are the effects and side effects of a2 agonists?

A

Beneficial- sedation, analgesia, muscle relaxant, ‘anaesthetic sparing’ agents
Side effects- deleterious CV effects- vasoconstriction increases after load, diuresis, hyperglycaemia, sweating
Antagonists available

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21
Q

What are the effects and side effects of acepromazine (phenothiazines)?

A

Sedation but less predictable, muscle relaxation, anaesthetic sparing, anti-emetic, long lasting, no analgesia
Side effects- vasodilation, paraphimosis, brachycephalic/exited animals have adrenalin reversal, anti-histamine, long lasting

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22
Q

What are the effects of butryophenones?

A

Sedation, muscle relaxation, anti-emetic, anti-histamine

Side effects- no analgesia, vasodilation

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23
Q

What are the effects of benzodiazepines?

A

Sedation, muscle relaxation, minimal CV effects
No analgesia
Side effects- can cause excitement if administrated on their own
Antagonists available

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24
Q

How can neurotransmitters alter the behaviour of animals?

A

Drugs are used to influence behaviour and emotional state- act by altering the efficacy levels of one or more neurotransmitters

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25
Q

What neurotransmitters can alter behaviour?

A

Serotonin- involved in regulation of mood, appetite, arousal, role in pain inhibition
Dopamine- major role in reward and pleasure, helps regulate emotional responses
GABA- main inhibitory neurotransmitter
Noradrenaline- helps form connections in the brain

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26
Q

What are the 5 main groups of psychoactive drugs?

A 
Tricyclic antidepressants
Specific serotonin reuptake inhibitors 
Monoamine oxidase inhibitors 
Benzodiazepines
Beta-blockers
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27
Q

What is the action of TCAs (tricyclic anti-depressants)?

A

Block the serotonins and noradrenaline transporters inhibiting reuptake, increases serotonin in synapses for longer

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28
Q

What are TCAs used to treat, what are the potential side effects?

A

Mainly used in anxiety disorders
Prolonged use down regulated 5-HT and NA receptors
Significant antihistamine, anticholinergic and alpha-1 agonist effect
Affects Na/Ca channels so should be avoided

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29
Q

What is the MOA of SSRIs (specific serotonin reuptake inhibitors), what problem occurs from overuse?

A

Inhibit uptake of serotonin
Overuse down regulates post-synaptic serotonin receptors
Less side effects then TCAs

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30
Q

What is the MOA of MAOIs (monoamine oxidase inhibitors)?

A

Monoamine oxidase is an enzyme found in many tissues including CNS
MAO A/B are involved in breakdown or serotonin, noradrenaline and dopamine
Only MAO B used in vet

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31
Q

What are beta-blockers used for and what do they cause?

A

Used in anxiety/anticipation scenarios
Reduce physiological signs of negative emotion states involving panic and stress
Central effect inhibits consolidation of memory

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32
Q

What are AEDs? (anti-epileptic drugs)

A

Can have applications in behavioural modification

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33
Q

Name 3 examples of TCAs?

A

Amitriptyline
Doxepin
Clomipramine- licensed in dogs

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34
Q

What is an example of an SSRI?

A

Fluoxetine- not authorised in UK

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35
Q

Name an example of a MAOI?

A

Selegiline is a MAO-B inhibitor for CCDS

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36
Q

Name an example of BZDs?

A

Alprazolam- non-licensed used in dogs

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37
Q

What is an example of a beta blocker?

A

Propanolol

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38
Q

Name 2 examples of AEDs?

A

Topiramate

Imeptoin

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39
Q

Describe the pharmacokinetics of TCAs?

A

Extensive first pass metabolism, highly protein boind, hepatically metabolised, bile excretion

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40
Q

Describe the pharmacokinetics of Fluoxetine?

A

First pass hepatic metabolism after oral admin, highly protein bound, hepatic metabolism, urine excretion

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41
Q

Describe the pharmacokinetics of selegiline?

A

Elimination half life 1 hour, hepatically metabolises to methylamphetamine

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42
Q

What can be used instead of drugs?

A

Pheromones- adaptil, feliway

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43
Q

What are the major classes of analgesic drugs?

A 
No plant
NSAIDs
Opioids
Paracetamol 
Local anaesthetics
Alpha 2 agonists
NMDA antagonists
Tramadol
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44
Q

What is the mechanism of action of NSAIDs?

A

Inhibit COX1- physiological and COX2 inducible (inflammatory)

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45
Q

What is the mechanism of action of opioids?

A

Receptors throughout the body, main analgesic effect is via the dorsal horn of the spinal cord, reduce exitatory neurotransmitter at nerve endings

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46
Q

What are the different types of receptors opioids effects?

A

Mu- analgesia
Kappa- sedation, some analgesia
Delta

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47
Q

What is the mechanism of action of paracetamol?

A

Precise mechanism not known- COX 1 inhibitor

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48
Q

What is the action of local anaesthetics?

A

Amides and esters- amides last longer

enter centres of axons and block sodium channels

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49
Q

How are each of the analgesics administered NO PLANT?

A

NSAIDs- IV, IM, SC, PO, Topical
Opioids- IV, IM, SC, PO, Topical, Transmucosal, Extradural, Synovial
Local anaesthetics- IV, Topical, Local infiltration, Transmucosal, Extradural, Perineurally, Synovial
NMDA- ketamine- IV, SC, IM, Transmucosal, Epidurla

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50
Q

What is the action of NMDA antogonists?

A

NMDA receptors involved in pain pathway in the CNS

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51
Q

What are the effects and side effects of NSAIDs?

A

Analgesia, Anti-inflammatory, Anti-pyrexia

Side effects- GI, renal (auto regulation of blood flow), Clotting, Liver, gastric ulceration

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52
Q

What are the effects and side effects of opioids?

A

Analgesia, sedation

Side effects- Bradycardia, respiratory ‘depression’, reduces GI motility, Excitement, Dysphoria, Vomiting

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53
Q

What are the effects and side effects of paracetamol?

A

Analgesia, anti-pyrexia

Side effects- Hepatotoxicity, Hypotension, No cats

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54
Q

What are the effects of local anaesthetics and the side effects?

A

Analgesia, Anti-inflammatory, anti-arrhythmic

Side effects- loss of effects of nerves, CNS toxicity, Myocardial toxicity

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55
Q

What are the effects and side effects of NMDA antagonists?

A

NMDA antagonists- Analgesia, ketamine- anaesthesia

Side effects- Excitement, Hypertonicity, myocardial depression, sympathetic stimulation

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56
Q

What drugs are used for chronic pain?

A

Gabapentin, amantadine, antidepressants

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57
Q

Name some examples of opioids that cause full Mu, Partial Mu, Mu antagonists/Kappa antagonists
What what is their antagonist?

A

Full Mu- Morphine, methadone, pethidine, fentanyl
Partial Mu- buprenorphine.
Mu antagonists/Kappa agonists- butorphanol.
Antagonists- Naloxone

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58
Q

What is an example of a local anaesthetics?

A

Lidocaine

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59
Q

List the injectable anaesthetic agents used in UK vets

A

Propofol
Alfaxalone
Thiopental
Etomidate

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60
Q

List the inhalation anaesthetics used in UK vets

A 
Isoflurane 
Sevoflurane
Halothane 
Desflurane 
Nitrous oxide
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61
Q

What are the advantages and disadvantages of injectable anaesthetic agents?

A

Simple equipment to administer
Once administered they need to be metabolised and excreted to be removed
Adjustment of doses to effect may be harder that inhalation agents

62
Q

What are the advantages and disadvantages of inhalation anaesthetic agents?

A 
Specialised equipment required
Easy to eliminate 
Easy to adjust depth 
Delivered in oxygen
Potential for environment contamination
63
Q

What is the MOA, administration and effects of propofol?

A

Gaba agonists
IV only- emulsion
Recovery due to distribution and hepatic metabolism
Effects- anaesthesia, sedation (low dose), muscle relaxation, anti-seizure
Side effects- Vasodilation, respiratory depression

64
Q

What is the MOA, administration and effects of alfaxalone?

A

GABA agonist
Neurosteroid with poor solubility, made water soluble IV, IM, SC
Recovery due to redistribution, hepatic metabolism
Effects- anaesthesia, sedation (low dose), muscle relaxation, anti-seizure
Side effects- vasodilation, respiration depression, excitable recovery

65
Q

What is the MOA, administration and effects of Ketamine?

A

NMDA agonist
IV, IM, SC, Transmucosal
Recovery due to redistribution/metabolism (excretion in cats)
Effects- anaesthetics, analgesia
Side effects- direct myocardial depression, increased HR, vasoconstriction, respiratory depression

66
Q

What is the MOA, administration and effects of Thiopental?

A

GABA agonists
IV
Redistribution recovery, slow hepatic metabolism
Effects- anaesthesia, muscle relaxation, anti-seizure activity
Side effects- myocardial depression, arrythmogenic, respiratory depression irritant extravascularly

67
Q

What is the mechanism of action of inhalation anaesthetic agents?

A

Not completely understood

68
Q

What is the MAC of an inhalation anaesthetic?

A

Minimum alveolar concentration- of an agent at which 50% of patients will not respond a % of atm

69
Q

What MAC is used for surgery?

A

1.2-1.5x MAC

70
Q

Side effects more pronounced around what MAC?

71
Q

What affects MAC?

A

Species, age, Low O2, other agents on CNS, catecholamines, pregnancy, low blood pressure, body temp

72
Q

What are the effects of sevoflurane and isoflurane, which is cheaper and more potent?

A

Effects- respiratory depression and potent vasodilation, anaesthetic
Isoflurane more potent and cheaper

73
Q

What is the triad of anaesthesia?

A

Muscle relaxation, unconsciousness, analgesia

74
Q

What is a seizure?

A

A transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain

75
Q

What are the 4 clinical components/phases of a seizure?

A

Prodromal, aura, lctus, post-ictal

76
Q

What happens during prodromal phase?

A

Before the seizure begins, behavioural changes occur such as wining or hiding- hours to days before

77
Q

What happens during aura phase?

A

First part of seizure, hours to minutes before, odd behaviour such as barking, pacing, salivating

78
Q

What happens during Ictus?

A

Proper seizure, involuntary muscle movement, twitches and changes in tone

79
Q

What happens during post-octal phase?

A

Period of time where the animal is disorientated, change in appetite, thirst, toileting

80
Q

What is classes as a an isolates seizure, a cluster of seizures and a status epilepticcus?

A

Isolates- 1 in 24 hours
Cluster- 2 or more in 24 hours
Status epilepticcus- last over 5 mins or repeated seizures

81
Q

Where do seizures occur in the brain?

A

Located in the forebrain

82
Q

What is the difference between a foal seizure and general?

A

Focal involves a specific site (cerebellum)

Generalised (both hemispheres)

83
Q

What are focal seizures associated with?

A

Focal disease process in the brain

84
Q

Which are the more commonly recognised seizure?

A

Generalised- classic tonic-clonic type- loss of consciousness, bilateral convulsions

85
Q

What can cause seizures?

A

Disease in brain

Disease outside brain- metabolic/toxic, still originates from the brain

86
Q

Why do seizures occur?

A

An imbalance of excitation and inhibition of neurotransmission in the brain
Can occur from excessive synchronous depolarisation of enough neurones in the brain will lead to a seizure (excessive excitation or insufficient inhibition)

87
Q

What forms an epileptic focus of pacemaker cells?

A

Groups of cells possessing an intrinsically high spontaneous firing activity

88
Q

Why do seizures need to be treated?

A

It causes damage to the brain and leads to increased pacemaker cells increasing seizure activity
Cluster seizure raises blood pressure and body temp rises to dangerous levels

89
Q

Successful treatment reduces seizures by what?

90
Q

What three broad categories are used for treat seizures?

A

Enhance GABA, Suppress Glutamate, Modulate movement of cations

91
Q

How are anti-epileptic drugs split?

A

First line and add on for further therapy

92
Q

Name the first line AEDs?

A

Phenobarbital
Potassium Bromide
Imepitoin
Diazepam

93
Q

Name the add on AEDs?

A 
Gabapentin
Pregabalin 
Levetiracetam 
Zonisamide 
Topiramate
Felbamate
94
Q

What is the MOA of phenobarbital, administration, half life and pharmacokinetics?

A

MOA- enhancing GABA-induces chloride ion conductance (hyperpolarising neuronal membranes)
Admin- Orally, IV
Half life- 24-40 hours takes 10-14 days for steady state
Phar- 50% is protein bound so don’t use with other highly protein bound drugs. Hepatically metabolised

95
Q

What is the MOA of potassium bromide, administration, half life, excretion?

A

MOA- enhances GABA induced Cl- conductance
Administration- oral but mucosal irritant
Half life- 25-46 days, 3 months to steady
Renal excreted- competes with Cl- ions
Not cats

96
Q

What is the MOA of Imepitoin, administration, half life?

A

Partial agonists at the benzodiazepine site of GABAa receptor- potentiates action of GABA
Oral administration- better on empty stomach
Half life- 1.5-2 hours, 3 days to reach steady

97
Q

What is imepitoin not recommended for and what can it be used with?

A

Not recommended for cluster seizures

Single agent of add on to phenobarbitone

98
Q

What is the MOA of diazepam, when is it mainly used for treatment of seizures, admin, what does it cause significant side effects in?

A

MOA- Benzodiazipine receptors activate the GABA chloride channel similar to phenobarbital
Appropriate sue in emergency treatment of seizures
Admin- IV or rectum
50% of cats have significant side effects

99
Q

What is the MOA of gabapentin, how is it excreted?

A

MOA- enhances GABA action, reduces glutamate activity, inactivate Na channels and reduce action of Ca channels
Renal excreted

100
Q

What is the MOA of Pregabalin, how is it excreted?

A

Structural analogue of GABA similar MOA to gabapentin

Renally excretes- minimal protein bound

101
Q

What is the MOA of levetiracetam, how is it excreted?

A

Main MOA decreases glutamate release- also enhances GABA mediated Cl- conductance
Rapidly metabolised
Renal excretion

102
Q

What is the MOA of Zonisamide and what are its pharmacokinetics?

A

Affects ion channels- reduction of flow through Ca channels
Long half-life
Hight protein bound
Hepatically metabolised

103
Q

What is the MOA of topiramate, how is it excreted?

A

Potentiales GABA activity

Renal excretion

104
Q

What is the MOA of felbamate and its pharmacokinetics?

A

Increases seizure threshold by reducing glutamate mediated exitation
High bioavailability
High protein bound
Metabolised by hepatic microsomal enzymes

105
Q

How can drugs be administered to the eye?

A

Topical can penetrate the globe, by crossing the cornea, conjunctiva or sclera or systemically by crossing blood:ocular barrier

106
Q

What are the advantages to topical administration of the eye?

A

Convenient
Easy and specific
Minimal side effects

107
Q

What are the tree ways topical eye drugs are distributed?

A

Drained by lacrimal drainage system, penetrates into eye cornea/sclera, enters systemic circulation through conjunctival and nasal mucosal vessels

108
Q

Why are drugs quickly removed from the surface of the eye?

A

Constant production, distribution and drainage of the pre-ocular film means drugs are removed rapidly

109
Q

Why do topical eye drugs need to have a certain osmolarity and pH?

A

If agents were irritant they would induce lacrimation and blinking

110
Q

Why do several drops of drugs to the eye need to be administered 10 mins apart?

A

Second drop will displace first reducing efficacy of both

111
Q

How can intraoccular bioavailability be improved?

A

Increasing the retention of the drug in the palpebral fissure or increasing its ability to penetrate the cornea

112
Q

How are ocular drugs supplied?

A

Supplied as ointments which contain an oily base, agent is either suspended/dissolved in base- reducing frequency of application

113
Q

Why has the agents used for eyes increased viscosity?

A

To increase retention, but beyond a certain viscosity would be irritant

114
Q

How can agents now use bioadhesion to increase retention?

A

Form a gel by binding to the mucin layer of the tear film

115
Q

How can topical drugs enter the eye?

A

Penetrate the cornea

Absorption through conjunctiva and sclera

116
Q

What is the first barrier to topical drugs entering the eye and what influences how easily drugs pass through?

A

Corneal epithelium

Lipid solubility

117
Q

How do most topical drugs enter the eye?

A

Through the cornea

118
Q

What is the second barrier of cornea to topical drugs and what influences what passes through?

A

Stroma- has high water content so facilitates diffusion of water soluble drugs, barrier to lipid soluble

119
Q

Why can both lipid and water soluble pass through the endothelium begin the stroma?

A

Is one cell thick and has gap junctions

120
Q

What do topical drugs that enter the eye therefore require in terms of properties?

A

Both hydrophilic and lipophilic characteristics

121
Q

What affects water solubility and lipid solubility of drugs entering the cornea?

A

Degree of ionisation

122
Q

How do most ophthalmic drugs exist in solution?

A

Weak acid/bases that exist in a balances solution of ionised and unionised forms

123
Q

Which is water soluble/ lipid soluble from ionised and un-ionised?

A

Water soluble- ionised

Lipid soluble- un-ionised

124
Q

How is a balanced solution of ionised and non-ionised form of a drug best for corneal penetration?

A

The un-ionised form crosses the corneal epithelium more easily. Once in the stroma the unionised drug ionises because of its abundance and more easily passes through the water high stroma. As it reaches the endothelium the ionised fraction is in abundance therefore more becomes un-ionised to cross the endothelium

125
Q

What affects the balance of ionised: unionised and how can this be disrupted?

A

The pH

Small variations in pH such as with infection can massively effect absorption

126
Q

What clinical factors affect corneal penetration?

A

Drugs can bind to protein in tear film- in inflammation increased protein in tear film
Damaged cornea- corneal ulceration will have increased corneal penetration of water-soluble drugs

127
Q

How can drugs be absorbed non-corneally?

A

Large hydrophilic molecules can still enter the eyeball, by absorbing across the conjunctiva and sclera
From conjunctiva the drugs can penetrate the eye via the sclera and enter the posterior segment or scleral vessels to the ciliary body

128
Q

How do topical agents systemically become absorbed into the eye?

A

Highly vascular tissue such as conjunctiva and the mucosa and nasopharynx enable absorption into blood stream

129
Q

How are eye topical drugs distributed and metabolised?

A

After cornea it moves into aqueous humour and to the iris and ciliary body
Lens and vitreous humour receive lower levels of corneally absorbed drugs
Drugs from non-corneal go to iris and ciliary body though blood supply

130
Q

How are drugs systemically administered to the eye?

A

Pass through the blood : ocular barrier which consists of the blood : aqueous barrier and blood : retinal barrier
Hydrophilic penetrate poorly, lipophilic readily, unless compromise

131
Q

Why is pupil dilation needed?

A

For better fundic examination

132
Q

What drugs cause dilation of the pupil?

A

parasympatholytics - relax the iris

Sympathomimetics- contract the dilator muscle

133
Q

What else can dilation drugs be used for?

A

To cause relaxation of the muscle in the ciliary body to relieve painful spasms in cases of anterior uveitis

134
Q

What are three examples of pupil dilators?

A

Atropine
Tropicamide
Phenylephrine

135
Q

What is the action, onset and length of action of Atropine?

A

MOA- parasympatholytic
Bitter tasting cause salivation
1 hour onset 120 hours acting

136
Q

How long does it take tropic amide to onset and last?

A

30 mins onset

Acts for 8-12 hours

137
Q

How long does it take phenylephrine to act and what type of drug is it?

A

10 mins of application

Selective alpha adrenergic drug

138
Q

What drugs actively increase tear production?

A

Parasympathomimetic- pilocarpine

Immunosupressant- ciclosporin

139
Q

What are the three categories of tear substitutes?

A

Aqueous, mucin, lipid

140
Q

What is the problem with aqueous substitutes?

A

Quickly lost from the ocular surface

141
Q

What is the most commonly used mucin later substitute?

A

Carbomer gel

142
Q

What is glaucoma?

A

Sustained increase in intraocular pressure

143
Q

What usually causes glaucoma?

A

Reduces aqueous humour flow

144
Q

How can glaucoma therefore be treated?

A

Increase outflow or reduce production of aqueous humour flow or both

145
Q

What are used as the first line of treatment of glaucomas and why?

A

Osmotic diuretics
Increase in blood tonicity causes water to be drawn out
Relies on intact blood:occular barrier

146
Q

What other drugs can be used to treat glaucomas?

A

Carbonic anhydrase inhibitors
Prostaglandin analogues
Beta-blockers
Parasympathomimetics

147
Q

How do carbonic anhydrase inhibitors treat glaucoma?

A

Catalyses the hydration of CO2 to bicarb and H+ in non-pigmented ciliary body of epithelium, bicarb moves into aqueous humour, water follows
Inhibition reduces production of aqueous humour

148
Q

Name two examples of carbonic anhydrase inhibitors used for glaucomas?

A

Brinzolamide

Dorzolamide

149
Q

How do prostaglandin analogues treat glaucoma and name an example?

A

Increase uveoscleral outflow of aqueous humour due to alteration in ultrastructure of outflow tract

Latanoprost

150
Q

How do beta blockers treat glaucoma and name an example?

A

Uncertain mechanisms

Betaxolol

151
Q

How do parasympathomimetics treat glaucoma and what is used?

A

Cause constriction of ciliary body and constriction of pupil- widens the drainage angle incease in outflow if intact
Pilocarpine used

Year 2 NSF (16 decks)

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