anaesthesia drugs and L-dopa Flashcards

1
Q

anaesthesia

A

muscle relaxation

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2
Q

muscle relaxants are

A

NMJ blockers - prvemt normal action of ACh

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3
Q

two types pf actions of muscle relaxants

A

depolarising and non polarisation

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4
Q

depolarising

A

e. g. succinylcholine
- 2 ACh joined together- antagonistic to AChr
- causes constant depolar

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5
Q

what metabolises succinyl choline

A

AChE

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6
Q

Non-depolarising

A
  • curare derivatives

- prevents ACh binding to the receptor

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7
Q

Opioids signal via

A

Gi/Go

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8
Q

Opioids and Gi/Go

A
  • decrease conc of cAMP
  • decrease conc of PKA- less phosphorylation of VOCCS
  • potassium channels open
  • less depolarisation
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9
Q

analgesia

A

inhibiting the feeling of pain

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10
Q

three opioid receptors

A

mu, delta , kappa - all responsible for diff roles

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11
Q

examples of opioids

A

codeine, diamorphine, tramadol

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12
Q

how do opioids prevent pain in dorsal horn

A

inhibition down from the brain to the spine

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13
Q

where do opioids work

A

site of injury- prevent inflammatory mediators from being released (allodynia)

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14
Q

ketamine

A

IV anaesthesisa

  • antagonises NMDA receptors
  • stopping glutamate from being excitatory
  • causing inhibitory state
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15
Q

Propofol/ thiopental

A
  • IV
  • Hypnosis effect
  • activates GABAa receptors
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16
Q

Propofol and GABAa

A

opens Cl- channels- hyperpolarisation- reduced excitability

17
Q

anticonvulsant drug

A

used for treatment of neuropathic prom
-enhanced GABAa

  • also blocks sodium/ calcium channels
  • reducing the release of excitatory glutamate
18
Q

local anaesthetic

A

produced anaesthesia by inhibiting excitation of nerve ending or by blocking conduction in peripheral nerves

  • achieved by reversibly binding to sodium channels- voltage gated
  • decreasing rate of depolarising and repolarisation
19
Q

local anaesthetic binds more readily

A

to activate Na+ channels- therefore neuronal blockade is fast in rapidly firing neurones
STATE DEPENDENT BLOCKADE

20
Q

seratonin

A

lack contributing to mood problems

-metabolised by MAOI

21
Q

negative of MAOis

A

associated with high BP

22
Q

L-dopa

A

dopamine is hydrophobic so cannot pass BBB

- L dopa used to treat parkinsons, to help increase control of movement due to death of DA neurones

23
Q

carbidopa

A

prevent l-DOPA from being converted to dopamine in the periphery

24
Q

COMPT inhibitors

A

prevents LDOPA from being converted to 3-O-mehtyldopa

25
Q

DCC

A

converted LDOPA to dopamaine

26
Q

MAO-B

A

converts dopamine to useless metabolites

27
Q

MAO-Is

A

selegilline

- prevents MAO from converting dopamine to useless metabolites

28
Q

Deep brain stimulation

A

a neurosurgical procedure where neurosimulator is implanted into he brain
-send s electrical impulses through implanted electrodes to specific targets in the brain

–> increases blood flow and therefore availability of NT

29
Q

antipsychotic

A

excess dopamine is associated with schizophrenia

  • these drugs have a high affinity for dopamine receptors
  • no depolarisation
  • can lead to symptoms of parkinsons