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Block 3: Brain and Behaviour > Guided learning- Anaesthetics > Flashcards

Guided learning- Anaesthetics Flashcards

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1
Q

3 a’s of conciousness?

A
  1. alertness -> upper brainstem reticular formation
  2. awareness -> cerebral cortex
  3. attention -> limbic system frontoparietal association areas
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2
Q

definitions:

normal

A

fully orientated time place and person

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3
Q

define sedation

A

allows patients to tolerate unpleasant diagnostic or surgical procedures

relieves anxiety and discomfort

verbal contact can be maintained

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4
Q

define coma

A

state of extreme unresponsiveness

individual exhibits no voluntary movement or behaviour

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5
Q

define anaesthesia

A

no concious awareness

patient without feeling or sensation

enters a drug induced and predictably reversible coma

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6
Q

define : concious sedation

A

patient relaxed and calm

able to undergo minor surgical procedures w/out too much discomfort

can maintain verbal contact

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7
Q

3 levels of sedation and effects

A
  1. minimal sedation
    • airway unaffected
    • CV function unaffected
    • normal responsiveness
    • spontaenous ventilation unaffected
    • reduced anxiety
  2. moderate sedation / concious sedation
    • no airway intervention
    • CV usually maintained
    • responsive to verbal and tactile stimulation
    • sponatenous ventilation is adequate
  3. Deep sedation (anaesthesia in UK)
    • Airway intervention may be required
    • CV function usually maintained
    • responsive to purposeful repeated or pain stimulation
    • spontaenous ventilation may be inadequate
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8
Q

3 scales of sedation?

A
  1. Ramsay (6 point)
  2. richmond sedation agitation scale (10 point)
  3. Riker sedation agitation scale (7 point)
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9
Q

Ramsay scale

aim?

levels

A
  • aim for level 2 -> cooperative, oriented, calm
  • 1 = agitated
  • 2 = aim 3 = Response to verbal
  • 4 and 5 = brisk / sluggish response to glabellar tap or loud auditory stimulus -> elicit blink reflex
  • 6= unresponsive
  • note unvalidated atm
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10
Q

Richmond scale

aim?

levels

A
  • 10 point scale with -5 being unarousable and +4 being combatitive/ violent to staff.
  • Aim for between 0 and -2:
    • -2 = light sedation, briefly awaken with eye contact to voice under 10 s
    • -1 = drowsy, not fully alert but sustained eye contact to voice more than 10 s
    • 0 = alert and calm
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11
Q

Riker sedation agitation scale

aim?

levels

A
  • 7 point scale
  • Aim : level 4 -> calm, coopertive, easily arousable, follows commands
  • 7 = dangerous agitation
  • 1 = unarousable
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12
Q

What is the aim in anaesthesia?

A
  • always aim for calm and relaxed
  • allows procedure to be performed
  • reduces agitation
  • if too sedated prolongs recovery and longer procedure time
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13
Q

Normal pupil sizes in light and dark ?

Pupillary responses during anaesthesia?

What is always checked for in the anaesthetised patient?

A
  • Light -> 2 -4 mm
  • dark -> 4-8 mm
  • Overdose -> FULL DILATION
  • Deep surgical anaesthesia (stages 2 - 4 ) -> 6-8 mm DILATED
    • brainstem function reduced
    • diaphragmatic respiration
    • eye and resp reflexes reduced
  • Light surgical anaesthesia (stage 3) -> MIOSIS, CONSTRICTED
    • PNS takes over
    • reflexes dampened
  • Analgesia (stage 1) -> 2-4 mm NORMAL
    • conciusness not sig. affected
  • Always check for pupillary light reflex and corneal blink reflex
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14
Q

What drugs are used for sedation

A
  • SEDATION = BOrED
    • Benzodiazepines
    • Opiates
    • Entonox
    • Dexmedetomidine
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15
Q

Name the benzodiazepines used in sedation

What is the MOA

A
  • Midazolam
  • Lorazepam
  • Diazepam
  • Temazepam

MOA: Binds Y subunit of GABAa receptor, PAM

increase affinity for GABA and freq of channel opening

increase Cl- conductance into cell

HYPERPOLARISES cell reduce AP firing

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16
Q

Benzodiazepines:

USES

SE’s?

A
  • Sedatives, muscle relaxants (hyperkinetic disorder)
  • anxiolytic and panic disorder
  • epilepsy
  • chronic insomnia

SE’s:

  • memory loss
  • no analgesia
  • decrease cog. function on recovery from sedation
  • prolonged use can result in tolerance and dependency
  • avoid in patients with heart/ resp/ liver problems or depressive / -ve sx.
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17
Q

Benzodiazepines:

reversal agent?

A

Flumazenil

(Shoo Benzo or ill give ya the FLU)

18
Q

OPIATES:

name 3 short acting used in sedation

MOA?

A
  • FENTANYL -> Short acting and strong
  • AFENTANIL
  • REMIFENTANIL

MOA:

Binds mu opiod R , GPCR (Gi/ Go)

Promotes opening Katp and Kir channels, inhibits opening VGCC and inhibit NT release via exocytosis block.

HYPERPOLARISATION via K+ efflux, and decreased NT release

Decrease neuronal transmission

19
Q

OPIODS:

1) cardinal signs of OD
2) reversal agent?
3) Adv’s?
4) adjunct to what?

A
  • Pinpoint pupils (miosis)
  • Respiratory depression
  • Coma

Reversal -> Naloxone (shorter acting antagonist) (Naltrexone longer acting)

Adv: good sedatives, analgesics, SM relaxants ,

adjunct to anaesthesia:

  • counteracts increase in CV and RR during invasive treatment
  • decrease dose of anaesthetic required as sedative effect
  • fast acting used as adjunct to prevent resp depression and OD
20
Q

SEDATIVES:

Name inhaled sedative

MOA

onset

adv’s

disadv’s

A

ENTONOX = Nitrous oxide 50: 50 mix O2 and N2O

Onset 2- 3 mins

MOA: unclear modulates range of R may induce opiod release

Adv’s: sweet smelling, non airway irritant, good analgesic

Disadv : potential teratogen, increase ear and lung pressures

21
Q

SEDATIVES:

Name sedative used in ICU

Moa?

A

Dexmedetomidine

Used in ICU for procedures when patient needs to maintain verbal contact

MOA: selective alpha2 adrenoR AGONIST

Binds presynaptic adrenoR to inhibit NA release and terminate pain signals

postsynaptically inhibits SNS -> reduce BP and HR

22
Q

3 main effects of anaesthetics?

Two main groups?

A

Unconciousness (Reticular formation and reticular activating system)

Loss of reflexes

Analgesia

Two main groups : 1) Local 2) General

23
Q

Name 3 local anaesthetics

Two groups and metabolism T 1/2

MOA?

A
  • LIDOCAINE (amide)
  • BUPVICAINE (amide)
  • LEVOBUPVICAINE (amide)

Two groups :

1) Amino Amides metabolism in LIVER, longer T 1/2 (3 Hrs)
2) Amino Esters metabolism in PLASMA, T 1/2 3 mins

MOA -> inhibit VG Na channel, dampends neuronal activity by inhibiting depolarisation, reduced sensory transmission to the cortex

Enter channel when open and by crossing PM and binding from the inside.

24
Q

uses and duration of:

Lidocaine

Bupvicaine

Levobupvicaine

A

Lidocaine: Nerve block, dental and topical procedures

duration 1-2 hours

Bupvicaine: regional IV anaesthesia, peripheral nerve block, epidural and SNS nerve block

Duration 1- 3 hours

Levobupvicaine: same as Bupvicaine (regional IV anaesthesia, peripheral nerve block, epidural and SNS nerve block)

Duration 1-3 hours

+ Less cardiotoxic than bupvicaine (would not used bupvicaine in HF patient)

25
Q

Local anaesthetics:

administration?

advantages?

side effects?

properties?

Limitations?

A

Admin : low dose and only affect small localised region

Adv: flexible, good recovery and few SE’s

SE’s: can get local irritation at site of admin, local ischaemia and traumatic admin can cause tissue damage

Properties: works best in small un or lightly myelinated neurons (Adelta or C fibres)

Limited by: Inflammatory soup, which is acidic. Leads to ionisation of basic and pH dependent LA drugs and inability to cross PM to bind to VG Na channel.

26
Q

Considerations w Local anaesthetics?

systemic effects w OD?

A

Agent with low irritant effect and toxicity

Half life adequate for procedure (amide in liver therefore longer T1/2, esters in plasma therefore T1/2 only mins).

Rapid onset of action

systemic effects OD: CV and CNS changes (cardiotoxicity and decreased conciousness/ sedation), anaphylaxis with esters

27
Q

Actions of General Anaesthetics?

A

reversible block nerve conduction

loss of sensation affecting whole body

loss of conciousness

28
Q

Two groups of GA?

List the GA’s

A
  • Inhalation and intravenous

PINKS

Propofol (IV because your veins are proper full)

Isoflurane

Nitrous oxide (entonox)

Ketamine (NMDA antagonist)

Sevoflurane

29
Q

Name the inhaled GA’s?

Adv’s?

Compared by what value?

A

Smoking is a SIN

Sevoflurane

Isoflurance

Nitrous oxide (entonox)

Adv’s: All have low solubility therefore rapid induction and few lingering effects.

Compared by their MAC value: mean alveolar concentration = conc of vapour required in alveoli to prevent motor response in 50% of patients to PAIN stimulus

30
Q

Potency, onset and recovery, uses of:

Entonox

Sevoflurane

Isoflurane

A

Entonox: Low potency, moderate recovery, onset 2-3 mins

Sevoflurane: onset and recovery moderate, exhaled and metabolised, day surgery, few SE’s

Isoflurane: Slow onset and recovery, half life from mins- hours, few adverse effects, widely used

31
Q

IV anaesthesia

induction?

use?

how do they suppress conciousness?

A
  • rapid induction in 30 s
  • used to induce generally, maintenance via inhalation or combination
  • not used alone due to accumulation and slow redistribution
  • suppress conciousness by decreasing CNS activity with inhibitory GABA and inhibiting excitatory Glutamate
32
Q

Name the IV GA’s?

A

Mates using KET are Proper Fools

Midazolam

Ketamine

Etomidate

Thiopental

Propofol

33
Q

Ketamine MOA , uses, SE’s

Midazolam MOA and uses

Thiopental MOA

A

Ketamine = NMDA glutamate R antagonist -> Blocks Na+/ Ca2+ channels

Uses: Analgesia and IM for short procedures

SE’s: hallucination raised HR/ BP on recovery

Midazolam MOA: Benzodiazepam GABA PAM at Y subunit

Uses: sedative and anxiolytic, short minor procedures w/out loss conciousness

Thiopental MOA: Barbiturate therefore GABA PAM at A/B subunits

34
Q

Etomidate: MOA, USES

Propofol: MOA, action/ uses

A

Etomidate:

MOA -> unclear

uses: induction without hangover

Propofol:

MOA -> unclear

Action/ uses -> maintenance, no accumulation therefore can have continous infusion

35
Q

Drugs for epidurals?

where is the injection (vertebral level) and what layers do you go through?

used for what procedures?

What scale used?

A

Lidocaine and Bupvicaine

Injection can be done at any vertebral level as entering the EPIDURAL space (between vertebral column and outer meningeal layer surrounding spinal cord) not the SUBARACHNOID space.

Differs from SPINAL anesthesia as spinal anesthesia enters subarachnoid space therefore alway done at L3/L4 to prevent damage to spinal cord.

Epidural goes through 1) skin 2) supraspinous ligament 3) infraspinous ligament 4) ligamentum flavum 4) epidural space

Used for genitourinary procedures/ Obs and Gyn/ Lower limb orthopaedics

Bromage Scale used

36
Q

What are the bromage scale levels

What does epidural block affect more motor or sensory?

is sensory fully blocked?

A
  • Bromage scale 0-3
  • O no block flexes knee and feet
  • 1 partial block, partially flexes
  • 2 almost complete block, inability to flex knees able to flex feet
  • 3 complete block -> unable to move legs or feet
  • Epidural affects sensory nerves over motor due lighter myelination and cold and pressure sensation not as affected.
37
Q

What adjuncts are used in anaesthesia and why?

What two groups are there?

Name them

A

Used NM blockers (muscle relaxants)

allows relaxation of skeletal muscles, allows relaxation of vocal cords to permit endotracheal tube.

Two groups: 1) Depolarising 2) non depolarising

Nervy anasethetists value Deep sedation nomatterwhat

Non depolarising = Atracurium and Vecuronium

Depolarising = Suxamethonium and Neostigmine

38
Q

Depolarising NM blockers

MOA

Reversal agents?

A

Suxamethonium : mimics ACh at NMJ (non competitive), hydrolysis much slower than Ach, prolongs depolarisation and overtime overloads the system -> leads to desensitisation

Neostigmine: Ach esterase inhibitor, prolongs Ach, inital depolarisation followed by desensitisation due to overloading system

reversal agents only exist for non depolarising, depolarising allowed to dissipate naturally.

39
Q

Non depolarising NMB’s

MOA

reversal agents?

A

Atracurium and Vecuronium MOA:

Competitively bind to and antagonise the AchR, prevent depolarisation

only takes 3-4 mins to max block, duration 40 mins

widely used due to fast onset

reversible by anticholinesterase (neostigmine) and suggamedex ONLY for Vecuronium. (remember by vencuronlyium w suggamedex).

40
Q

Reversal agents MOA

A

Neostigmine -> inhibits anticholinesterase breakdown, increases conc of Ach in cleft to compete with the non depolarising blocker, allow activation of Ach channels again.

Suggamedex -> oligosaccharide that forms a complex w vecuronium, promotes removal from NMJ and into plasma

Block 3: Brain and Behaviour (14 decks)

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