Anaesthetic teaching Flashcards
1
Q
Different types of anaesthesia
A
3 different types
general anaesthesia
regional anaesthesia
local anaesthesia
2
Q
what is general anaesthesia
A
total loss of sensation
3
Q
what is regional anaesthesia
A
loss of some sensation to a region or part of a body
4
Q
what is local anaesthesia
A
topical agent to infiltrate the superficial area of the body
5
Q
what are the 3 different steps required to achieve full loss of sensation
A
Amnesia - unconsciousness and memory loss
analgesia - pain relief
akinesia - immobilisation/paralysis
6
Q
what is the preparation required pre-GA?
A
patient needs to be fasted to reduce risk of aspiration during anaesthesia –> which is a major risk of death for anaesthesia
7
Q
what does a typical monitoring machine have on display?
A
ECG (3 leads)
SpO2 (peripheral O2)
NIBP - non-invasive BP
airway gases - O2, CO2, vapour
airway pressure (to ensure airway potency)
nerve stimulator (if muscle relaxant used and required to check nerve innervation)
temperature (required for anybody whose operation is > 30mins)
8
Q
what is arm-brain circulation time
A
time taken for medication to travel from brachial vein to the brain (which is how long it will take induction medication of anaesthesia to work)
10-20 secs
9
Q
what long does induction agents usually last
A
4-10 minutes
10
Q
use of inhalation agents?
A
to maintain amnesia in a prolonged operation (otherwise, induction agents are good enough)
11
Q
what is the most commonly used induction agent
A
propofol
12
Q
why is propofol the most commonly used induction agent
A
excellent suppression of airway reflexes –> stops reflexes from airway insertion
13
Q
which induction agent is mainly used in rapid induction sequence
A
Thiopentone
14
Q
how quickly does etomidate work?
A
rapid (much quicker than propofol)
15
Q
what is the normal dosage of etomidate
A
0.3mg/kg
16
Q
what does etomidate cause haemodynamically
A
stable - does not raise or drop HP/BP
17
Q
SE of Etomidate
A
pain on injection
spontaneous movement
adreno-cortical suppression (a single dose cause adrenal suppression for 72 hours, so never use in critically ill patient)
high incidence of PONV
18
Q
what type of patient would benefit from etomidate
A
cardiac patient
19
Q
which induction agent cause dissociative anaesthesia
A
ketamine
20
Q
what is dissociative anaesthesia
A
it causes patient to have a mystical or g spiritual experience during ketamine use
21
Q
which induction agent causes memory problem
A
ketamine causes anterograde amnesia
22
Q
what is anterograde amnesia
A
it is the inability to form new memory from injection of ketamine
23
Q
what is the dosage of ketamine
A
1-1.5 mg/kg
24
Q
how quick is the onset of ketamine
A
slow 90 seconds
25
SE of ketamine
raise in HR, Raise in BP
Bronchodilation
N+V
emergence phenomenon - vivid dreams, hallucinations
Anterograde Amnesia
Dissociation Anaesthesia
26
what is the dosage of propofol
1.5-2.5mg/kg
27
rate of PONV and propofol?
dec rate
28
SE of propofol
mark drop in HR and BP
pain on injection
involuntary movement
29
dosage of thiopentone
4-5 mg/kg
30
when is thiopentone mainly used?
rapid sequence induction
31
SE of thiopentone
raise in HR
drop of BP
rash/bronchospasm
intra-arterial injection (can lead to thrombosis and gangrene
32
when is thiopentone contra-indicated in?
prophyria
33
which of the inhalation agent has the least affect on organ blood flow
Isoflurance
34
which inhalation agent is used for organ retrieval from a donor
isoflurance
35
which inhalation agent is used for paediatric patient
Sevoflurance (S for small patient)
36
which inhalation agent is used for inhalational induction
Sevoflurance
37
what inhalation agent has the least duration?
Desflurane (low lipid solubility - less Desflurance is absorbed into fat and muscle and so less time taken to vent off post op)
38
which inhalation agent is most suitable for long-operation such as finger -replantation
Desflurane
39
What induction agent is used solely for short procedure?
ketamine
40
what are the 2 different methods of maintaining amnesia
1) propofol - IV infusion
| 2) inhalation agents via inhalation
41
What is the definition of minimum alveolar concentration (MAC)
minimum concentration of vapour required to prevent reaction to standard surgical stimulus in 50% of patients
42
what is the MAC for nitrous oxide
104%
43
mac for isoflurance
1.15%
44
MAC for enflurance
1.6%
45
MAC for sevoflurane
2%
46
MAC for Desfluane
6%
47
which induction agent has anti- epileptic and brain protective characteristic?
Thiopentone
48
how many different types of analgesia required to maintain pain free for patient post- op
2 types
short and long acting
49
why is analgesia required during anaesthesia
for management of pain of inserting an airway/LMA/intubation/intra-operative pain relief/poster-operative pain-relief
50
when is short acting analgesia used?
intra-op - to suppress response to laryngoscopy + surgical pain
51
what are the different medication of short acting analgesia
remifentanil > alfentanil > fentanyl
in descending order of potency and duration
52
which short acting analgesia is most commonly used
Fentanyl
53
when is long-acting analgesia used in the whole of anaesthesia process
intra-op and post-op
54
what are the most commonly used long-acting analgesia for anaesthesia
morphine and oxycodone
55
what are the other analgesia used during anaesthesia
paracetamol Iv
| NSAID - Disclofenac, Parecoxib and Ketorolac
56
which of the NSAIDs are available in IV form
Parecoxib and Ketorolac
57
what are the weaker opioids used in anaesthesia
tramadol and Dihydrocodeine
58
Main type of akinesia agents?
Depolarising and Non-depolarising
59
how does depolarising akinesia agent work
act similarly to ACh and binds to the nicotinic receptors - -> v. slowing breakdown by ACheasterase --> causes muslce contraction/fluctuance initially, then muscle fatigues and relaxes
60
what are one fo the most complained SE of depolarising akinesia agent
Flu-like symptoms due to breakdown of muscle during the initial contraction
61
how does non-depolarising akinesia agent work
block the nicotinic receptors acting as a competitive inhibitor
62
what is an example of depolarising agent
Suxamethonium
63
dosage of Suxamethonium
1-1.5 mg/kg
64
when is Suxamethonium used specifically
in rapid sequence induction
65
SE of Suxamethonium
```
muscle pain
fasciculations
hyperaemia
malignant hypertension
Rise in ICP, IOP and gastric pressure
```
66
How many different types of non-depolarising akinesia agents are there
3
```
short acting (30 mins)
intermediate acting (45 mins)
Long (60 mins)
```
67
examples of short acting non-depolarising akinesia agent
Atracurium, Mivacurium
68
examples of intermediate acting non-depolarising akinesia agent
Vecuronium, Rocuronium
69
examples of long acting non-depolarising akinesia agent
Pancuronium
70
How can akinesia be reversed
using Neostigmine & Glycopyrrolate
71
how is the maintenance of BP achieved intra-operatively
Vaso-active agents
mainly to treat hypoTN
72
what are the commonly used vaso-active agent?
ephedrine
phenylephrine
metaraminol
noradrenlaine
adrenaline
bobutamine
73
effect of ephedrine
rise HR and contractility --> leads to inc BP
inc BP
inc HR
(a&B receptors)
74
effect of phenylephrine
rise BP by vasoconstriction but dec HR
Inc BP
Dec HR
a receptor mainly slight b receptor
75
effect of metaraminol
In in BP by vasoconstriction
inc BP
- HR
pre a receptor
76
when is noradrenaline, adrenaline an dobutamine most commonly used?
severe hypoTN/ ICU
77
why do we need to give anti-emetic as part of analgesia pathway
to prevent PONV caused by induction agent, vaso-active agent and analgesia analgesia
78
what are the commonly used anti-emetic?
5HT3 bloker --> ondansetron
anti-histamine --> cyclizine
steriods --> dexamethasone
phenothiaizine --> prochlorperazine
anti-dopaminergic --> metoclopramide
79
how would do reverse the action of anaesthesia - mainly muscle relaxant?
top anaesthetic vapours
give 02
perform throat suction
reverse muscle relaxation --> neostigmine + Glycopyrrolate
80
MOA of neostigmine
anti-cholinesterase, prevent breakdown of ACh but has muscarinic effect of ACh (bradycardia etc)
81
why do we need glycopyrrolate
it is an anti-muscarinic agent which conteract the muscarinic effect of neostigmine
82
definition of local anaesthetics
reversibly prevents transmission of the nerve impulse
in the region to which it applied
without affecting consciousness
83
types of local anaesthetics
2 main types
Ester
Amide
84
why would you prefer to use Amide rather then ester
ester less stable in solution and so can not be stored as long as amide so amide more commonly used
ester metabolised to PABA which has a higher association to allergic reaction but amide rarely cause any allergic reaction
85
different types of ester LA
short acting --> procaine, benzocaine, cocaine
medicaum acting --> prilocaine
long-acting --> amethocaine
ABC+P
86
different types of amide LA
medium acting --> lidocaine, mepivacaine
long acting --> Bupivacaine, levobupivacine, ropivacine
anything else (Bupi)
87
how many neurons are required to pass on an pain signal
3
88
different types of LA
topical local
nerve block
epidural
spinal
89
main principle of MOA of medication used in LA?
by inhibiting the voltage sensitive Na+ channel in axon preventing AP from firing
this cause a reversible block of conduction along the nerve fibre ie stopping the pain signal being ever received in the brain
therefore, LA has membrane stabilising affect
90
Step of the WHO analgesia ladder?
pain intensity 0 --> PRN parce
pain intensity 1 --> regular + PRN weak opioids/NSAID
Pain intesnity 2 --> regular prace + reg weak opioids + reg NSAIDs + PRN strong opioid
pain intensity 3 --> reg parace + reg NSAIDs + PRN strong opioids or + standard PCAS/epidural/single shot spinal
91
how does LA exert toxicity?
by blocking Na+ channel which are found in the brain and heart
92
what are some manifestation of toxicity of LA
lightheadedness, tinnitus, circumoral and tongue numbness
musclar twitching, visual disturbances
unconsciousness, convulsions
coma
resp arrest
CVS depression
93
what affect the sequence of system involvement of LA toxicity
route of injection and dosage
94
what system is affected first if the plasma level of LA rise slowly
CNS --> excitatory due to inhibition of GABA receptors
at higher plasma level --> widespread Na+ channel blockade with more generalised neuroonal depression --> coma and resp and CVS depression
95
management of LA toxicity
stop LA injection
call for help
ABCDE
aim --> maintain airway (if necessary secure with tracheal tube), give O2, IV access, control seizures with benzodiazepine, thiopental
96
definitive treatment for LA toxicity
IV lipid emulsion
97
dosage of lidocaine
3mg/kg
98
dosage of lidocaine with adrenaline
7mg/kg
99
dosage of bupivacaine
2mg/kg
100
dosage of bupivacaine with adrenaline
2mg/kg
101
dosage of Levobupivacaine
2mg/kg
102
dosage of Levobupivacaine with adrenaline
2mg/kg
103
dosage of prilocaine
6mg/kg
104
dosage of prilocaine with adrenaline
8mg/kg
105
definition of pain
an unpleasant sensory and emotional experience
associated with actual or potential tissue damage
or described in terms of such damage
106
what are the different types of pain ?
acute
chronic
cancer
107
what is the main cause of acute pain
trauma or noxious stimuli, disease process, abnor function of muscle/viscera
108
what are the main causes of chronic pain
nociception, psychological and behaviourla facros plat major part
109
what can post-operative pain cause
CVS - tachycardia, hypoTN, inc myocardial demand
RS - dec vital capacity, dec functional residual capacity, basal atelectasis, resp infection
GI - N+V, ileus
Other - PE, DVT
110
what is A fibre
myelinated, fast pain afferent portion of the reflex arc associated with pulling away from noxious stimulus
111
what is C fibre
unmyelinated slow fibre associated with slow, dull and longer lasting pain
112
what are most pain recepetors
nociceptor - free nerve ending whch sense heat, mechanical and chemical damage
113
what is a mechanoreceptors
respond to pinprick and pinch
114
what is a silent nociceptors
respond only in presence of inflammation
115
what is a polymodal mechanoheat nociceptors
most prevalant and respons to excessive pressure, extremes of hreat <42 >18 degree and allergens or pain producing substances
116
what are allergens
bradykinin, histamine, serotonin, H+, K+ and prostaglandins
117
course of action of nociceptors
when a cell is damaged - histamine and bradykinin is released
phosopholiase A2 is activated and converted into prostaglandins
prostaglandins then warren the firing of AP in the nerve endings
118
analgesia mode of action
transmitter of nerual signal from spinal cord to brain are conducted by 5HT (serotonin) or noradrenalien
so drugs affecting these 2 neurotransmitter can affect pain control by altering descending pathways and ascending pathways
119
which pathwya does Opioids, amitriptyline, tramadol and clonidine affect?
ascending pathway
120
which pathway does paracetamol affect
descending pathway
121
how does paracetamol work
inhibits COX2 mainly which metabolise prostaglandin and hence produce a signal in nerves
122
dosage of paracetamol
10-20mg/kg up to 1 g
can be repeated 4 times a day (4g max)
123
MOA of NSIADs
COX inhibitors both COX 1 and COX 2 (COX 2 = theraputic ability, COX-1 = SE)
124
which of the NSAIDs are more COX-1 selective
ibuprofen, disclofenac
125
which of the NSAIDs are more COX-2 selective
parecoxib, celecoxib
126
what are examples of weak opioids
codeine, dihydrocodein, tramadol
127
dosage of tramadol
50-100mg 4-6 hourly
128
what are 2 characteristics of pain suggest chronic pain
sharo/shotting or buning
129
definitino of. chronic pain
persistent and intractable pain lasting ? 3 months
130
what is neural plasticity
pain experience beyond area of original injury
131
what is Allodynia
normally light touch generating an non-proportional pain
132
what are some of the medication used to manage chronic pain
conventional analgesia
antidepressanys - amitriptyline (control serotonin)
antiepileptics - phenytoin, carbamazepine, sodium valporate, gabapentin
clonidine - alpha 2 agoinst
ketamine
corticosteroids - dexamethasone
capsaicin - affect c fibres and depletes substance P
