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VSCI200 NSF > export_neuro pharm > Flashcards

export_neuro pharm Flashcards

1
Q

What is the visual axis?

A

A line from greatest curvature of eyeball. And passes through area centralis.

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2
Q

Describe the optic nerve

A

Exits ventromedialy from the bulb. Deccusates at optic chiasm.

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3
Q

Name different types of calcium channels?

A

L type - slows, sustained
N type

T type - fast

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4
Q

Inc intracellular calcium of the pre-synaptic neurone results in…

A

NT release into synaptic cleft

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5
Q

Name 3 NTs?

A

ACh
Glutamate

GABA

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6
Q

Why does smokig only act in the brains AChR not muscles?

A

Because the nicotinic AChR are different

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7
Q

What does AChE break ACh into?

A

acetate and choline

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8
Q

What bdown ACh in the blood?

A

Pseudocholinesterases

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9
Q

What is organo-phosphates primary action?

A

To inhibit AChE and pseudo-ChE

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10
Q

Describe the uptake of MA into the pre-syn neurone

A

Uptake of whole molecule by MA transporters. Cleaved by MAO within cell.

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11
Q

What NT is primarily responsibel for inhibitry PSP in the brain?

A

GABA

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12
Q

What is the difference between nicotinic and muscarinic ACh R?

A 
Muscarinic = G-protein and either excitatory OR inhib
Nicotinic = Ion channels
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13
Q

Name and describe the 2 GABA Receptors?

A 
GABA-A = ion channel
GABA-B = g protein
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14
Q

Describe the action of the following drugs on GABA-A R.
a. Benzodiazepines

b. neuroactive steroids
c. barbituates

A

a. activate channel
b. facilitate opening

c. potentiate GABA-A action

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15
Q

What is the difference between pain and nociception?

A

Pain is when nociceptive stimuli is processed in the brain

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16
Q

Describe polymodal pain receptors

A

Stimulus causes ion channels the open along pain pathway.

Ruffini receptors.

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17
Q

Describe the spinothalamic pain pathway

A
  • peripheral afferent pain fibre enters Dorsal horn
  • processed in laminae 2 in substantia gelatinosa which releases substance P
  • synapses and decussates to contralateral spinothalamic tract
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18
Q

Name the 2 parts of the ventrolateral tract#

A

spinoreticular and spinothalamic

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19
Q

describe the spinoreticular tract

A

True pain

run up ventrolateral tract until the reticular formation in the medulla

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20
Q

What is the spinocervical?

A

Similar to spinothalamic, detects flea
tract asc in lat funiculus

decussates at level of lat cervical nucleus

asc in medial lemniscus to thalamus

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21
Q

Describe the pain gate

A

Desc fibres from PAG release serotonin @ pain gate
this paingate neurone releases enkaphalins

these inhib transmission of pain from C fibre to 2ry pain afferent to spinothalamic tract

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22
Q

What is r eferred pain

A

pain is felt in a particular site but originates elsewhere

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23
Q

What is phantom limb pain?

A

perceived sensation of amputated limb. Due to random firing of withdrawn nerve fibres.

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24
Q

What is hyperalgesia

A

sensitisation from inflammation.

spinal cord re-wiring

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25
Q

Anti-dromic neurotransmission is..?

A

pain is detected and stimulates more chemoreceptors to be released, exacerbating the issue.

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26
Q

What is the difference between sedative and tranquilisers?

A 
Sed = calm, dowsy leads to sleep
Tranq = calm, alert leads to catalepsy (unresponsive)
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27
Q

Name the 4 classes of sedatives in Vet Med?

A
  1. Benzodiazepines
  2. A2- agonists
  3. Phenothiazines
  4. Butyrophenones
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28
Q

Describe BZD therapeutic properties

A

1) muscle relaxant
2) anxiolytic

3) anti-seizure
4) amnestic

NB NO analgesia!

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29
Q

What does MADME stand for?

A

M - mechanism
A - absorption

D - distrubution

M - Metabolism

E - elimination

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30
Q

What is the 1st Pass metabolism?

A
  • immediate toxin (drug) removal

* via heptic portal vein before enters b. stream

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31
Q

Name a BZD reversal agent?

A

Flumazenil

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32
Q

What are the different function of alpha 1 and 2 receptors?

A 
A-1 = smooth m contraction eg blood vessels (stim by NA)
A-2 = smooth m contraction AND at neurones inhib of NA effects
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33
Q

Describe effects on A-2 receptors

A

Neurone releases NA –> attatches to A1 receptor = vascon of vessel (eg)
NA in synapse feedback to A2R on pre-sy terminal = inhib NA release

Dec NA release –> stops vasocon and other smooth m contraction and reduces B1 effects (eg HR)

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34
Q

Why are A2 agonists desired in sedatives?

A
  • red HR
  • muscle relaxant
  • analgesic properties
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35
Q

What are the side effects of A2 agonists?

A

CV depression –> hypotension (partic as HR reduced!)

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36
Q

Name 3 a2 agonists

A
  • xylazine
  • medetomidine
  • detomidine
37
Q

Name a A2 antagonist (reversal)

A

Antipamezole (wild upon waking) and reverses analgesia too!

38
Q

What are the properties of phenothiazines?

A
  • wide antagonist action:
  • D2
  • Muscarinic cholin
  • Histomine
  • Alpha 1
  • Dopamine ! neuroleptics
39
Q

Name 2 Phenothiazines

A

ACP (ace promazine)

Chlorpromazine

40
Q

Negative side effects of Phenothiazines

A
  • NO ANALGESIA
  • anticholin (dry mouth etc)
  • enhance narcotic effects of other drugs
  • tremor common
  • hypotention/hypothermia
  • incoordination
41
Q

Name 2 classes of sedative which are also anti-emetics

A

Phenothiazines and Butyropherones

42
Q

Name a Butyropherone

A

Azaperone (Stresnil)

43
Q

Describe the inputs involved in emesis

A 
Pain pathway (histamine) + Vestibular (ACh) = immediate sickness
CTZ (chem trigger zone in 4th ventricle) is dopamine path = poorly or alcohol induced.
44
Q

Why is dopamine often targeted in sedatives?

A

Lots of dopamine R in basal ganglion (involved in movement)

45
Q

What are the main functions of local anaesthetic (exc pain relief)

A

reduce need for GA, diagnosis of situation of pain

46
Q

What are LA (local anaesthetics) often combined with?

A

Vasoconstrictors to prevent spread of analgesia (often adrenaline)

47
Q

What is polymodal pain control?

A

When multiple nociceptors are target either by a single drug or a combination.

48
Q

Name 3 local anaesthetics

A

Lidocaine
Mepivicaine

Bupivicaine

49
Q

What LA is toxic, causes vasocon with a very long half life??

A

Bupivicaine

50
Q

Why do LA target pain fibers over motor fibers?

A

Unmyelinated and thinner so easier to act on.

51
Q

MiLK is used fo anaesthesia of horses, what does it contain?

A

Morphine, Lidocaine and Ketamine

52
Q

Describe the major properties of opioids

A
  • analgesics
  • narcotics
  • anti-diarrh
  • anti-tussive
  • sedation or excitment
  • nausea
53
Q

Name 3 opiods, excluding morphine

A
  1. Fentanyl
  2. Pethidine
  3. Buprenorphine
54
Q

Buprenorphine is.

A
  • slow on and offset

- mixed agon/antag

55
Q

What 3 opioids are mu agonists?

A
  • fentanyl
  • morphine
  • pethidine
  • etorphine is a mu and kappa agonist!
56
Q

What opioid receptors do Buprenorphine and butorphenol ANTAGonise?

A

Muu

57
Q

What opioid receptor do buprenorphine and butophenol AGONise?

A

Kappa

58
Q

What opioid is a D, M and K antagonist?

A

Naloxone

59
Q

Which type of opioid results in a ‘ceiling effect’ over a certain dose.

A
  • Ag-antag opioids

* (buprenorphine and butorphenol) High affinity @ mu and kappa receptors top-ups inc side effects, not analgesia

60
Q

Why would you use a opioid antag such as Naloxone?

A

Reversal if OD

61
Q

Describe the opioid receptor G-pCR mechanism

A
  • OpR bound to Gprotein
  • Op binds, GDP dissociates
  • GTP replaces it
  • opioid detatches
  • 2nd messanger
  • intracellular changes and effects
  • inhib Subs P, ACh and NA
62
Q

There are three opioid intracellular mech of action

A
  • dec Ca++ entry
  • inc efflux of K+
  • Inhib Adenylate cyclase
63
Q

Mu receptor agonists action in the dorsal horn is..

A

to prevent Ca++ influx and so supress substance P release. (GABApentine does same!)

64
Q

Fentanyl + ACP =

A

sedative

65
Q

What opioid is used in immobilisation fo large game?

A

Etorphine

66
Q

Name a drug that will reverse resp depression (can be caused by opioids)

A

Doxapram (analeptic) and DOESN’T reverse analgesia

67
Q

Name a NMDA blocker

A

Amantadine

68
Q

What are the aims of balanced anaesthesia

A
  • sleep
  • immobilisation
  • analgesia
  • muscle relaxant
69
Q

Name 3 classes of injectable induction agent

A
  • Ketamine
  • Barbituates
  • Propofol
70
Q

Name 3 barbituates

A
  1. Pentobarbitone
  2. Phenylbarbutol
  3. Thiopentone
71
Q

Therapeutic index (TI)

A

The ratio of the dose of the drug that is toxic to humans as compared to its minimum effective (therapeutic) dose.

72
Q

Why do barbituates give a nasty after effect?

A

Stores in fat, where it is then slowly metabolised

73
Q

Propofol properties

A
  • GABAa R = target
  • CV depression
  • safer than thiopentone
74
Q

Ketamine properties

A
  • eyes open
  • NMDA-R
  • V++ analgesic
  • INC muscle tone
  • INC salivation
75
Q

What are neuroactive steroids

A

Progesterone derviative which target GABA receptors. Good for tonic inhibition.

76
Q

Name a neuroactive steroid used in Pharmaceuticals?

A

Alfaxalone

77
Q

Alfaxalone properties

A
  • GABA-ergic agon
  • no inj pain
  • liver metab; urinary excretion
  • NO analgesia
  • less CV depression than propofol
78
Q

Name 4 inhalation maintenance agents:

A
  • Iso
  • Sevo
  • halo
  • N20

(Ether)

79
Q

What is 5mmol in mBar?

A

50mBar

80
Q

What is the speed of a volatile anaesthetic is dependant on…

A

lipid solubility (more lipid sol the better potency)

81
Q

What is the MAC

A

Minimal alveolar concentration

82
Q

What is MAC definition?

A

concentration to cause sleep in 50% of the animals.

83
Q

What is the benefits of sevofluorane?

A

Non-teratogen, low blood solubility and 100 % excreted by lungs (same as iso)
- more potent

  • quicker action
  • need expertise!
84
Q

Why is halofluorane no longer used?

A

teratogenic

85
Q

Why would N2O be used?

A

Good analgesia
V swift to act

No sleep as not potent enough

86
Q

What is diffusion hypoxia?

A

Seen in N2O, if turned off it moves so swwiflt from the blood into the lungs other gases cant enter lungs fast enough. NOs cause bronchconstr = hypoxia

87
Q

What is the 2nd gas effect?

A

N2O moves into blood so rapidly the concentration of other gases relative the N2O will increase!

88
Q

How do you verify death?

A

Heart
CN

Vital signs

Reflexes

89
Q

Name 3 methods of euthanasia

A
  1. Gas - welfare concerns with panic with poorly controlled CO2/CO levels
  2. Inj - IV best. Pentobarbitone w/ local anesthetics as stings.
  3. Gun - medullar oblongata

VSCI200 NSF (25 decks)

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