Studying this sux

Question 1

What are the 3 different GABA receptors and their role in the body?

Answer 1

A = neuronal excitability, rapid mood changes, anxiety and sleep
B = memory, mood and analgesia
C = unclear

Question 2

How is hyoscine butybromide used clinically?

What is it mechanism of action?

Answer 2

Colicky abdominal pain due to obstruction or increased respiratory secretions
MoA = anti-muscarinic

Question 3

Are C fibres inhibiting or stimulating for pain?

Answer 3

C fibres = inhibiting

Question 4

What does SLUDE stand for and what are it’s cause’s?

Answer 4

Salivation, Lacrimation, Urination, Defecation and Emesis 
Drug overdose (anti-cholinergics) or nerve gas

Question 5

What area of the brain are the central chemoreceptors located in?
What do they respond to?
Where are the peripheral chemoreceptors?
What has a stronger influence on respiration rate?

Answer 5

Medulla
Indirectly CO2 which diffuses across and then is converted into H+
Aortic and carotid bodies
Medulla > aortic/carotid

Question 6

What is the pathology of malignant hyperthermia?
What sort of genetic condition is it?
How is it treated?

Answer 6

Intracellular Ca++ transport is deranged via RYR protein mutation causing sustained muscular contractions which generate heat, C02 and hyperkalaemia
Autosomal dominant
Treatment = Dantrolene

Question 7

what is the mechanism of action?
Paracetamol?
Paed dosing?

Answer 7

prostaglandin inhibitor
15mg/kg every 4 hours

Question 8

How does Fentanyl and Morphine differ in their actions and routes?

Answer 8

Fentanyl = mu opioid receptor agonist in addition to kappa and delta-type receptors. Can be given transdermal or intravenous 
Morphine = mu opioid receptor agonist. Can be given intravenous, subcutaneous, rectal, intramuscular or oral

Question 9

Propofol moa?

Answer 9

Moa = decreases the rate of dissociation of the GABA from the receptor, thereby increasing the duration of the GABA-activated opening of the chloride channel with resulting hyperpolarization of cell membranes.

Question 10

Propofol:
Half life?
Onset of action?
Metabolism?

Answer 10

Half life = 2-24hrs
Onset of action = 5-10mins
Metabolism = liver glucuronidation

Question 11

Intubating dose of sux?
Onset?
Duration?
Moa?

Answer 11

1mg/kg
30-60seconds (43seconds)
3–5mins
Moa = agonist, binds directly to post-synaptic ACh receptors at motor end plate, causing continuous stimulation.

Question 12

ROCURONIUM 
Intubating dose? Elective vs RSI
Onset?
Duration?
Maintenance dose?
Moa?
Reversal?

Answer 12

0.6mg/kg OR 0.9mg/kg
90secs OR 60secs
20-30mins OR 30-40mins
Maintenance = 10-15mg  
Moa = competitive antagonist to acetylcholine at nicotinic receptors at motor end plate 
Neostigmine

Question 13

What conditions increase the risk of using suxamethonium?

Answer 13

Burns
Hyperkalaemia (renal disorders)
Neuromuscular disorders
Immobility 
Denervation injuries (spinal cord)

Question 14

Extensive explanation of suxamethonium:
binding site
Action vs normal muscle contraction
Breakdown?

Answer 14

Binding of suxamethonium to the nicotinic acetylcholine receptor results in opening of the receptor’s cation channel; a disorganized depolarization of the motor end-plate occurs and calcium is released from the sarcoplasmic reticulum.
In normal skeletal muscle, acetylcholine dissociates from the receptor following depolarization and is rapidly hydrolyzed by the enzyme acetylcholinesterase. The muscle cell is then ready for the next signal.
Suxamethonium has a longer duration of effect than acetylcholine, and is not hydrolyzed by acetylcholinesterase. By maintaining the membrane potential above threshold, it does not allow the muscle cell to repolarize.

Question 15

How does Suxamethonium cause paralysis and not tetany? re: calcium

Answer 15

Calcium is removed from the muscle cell cytoplasm independent of repolarization. As the calcium is taken up by the sarcoplasmic reticulum, the muscle relaxes. This explains muscle flaccidity rather than tetany following fasciculations.

Question 16

Vecuronium vs pancuronium
Dose?
Onset?
Duration?

Answer 16

Both = 0.1mg/kg 
Onset = V 90secs  P 90-120secs 
Duration = V 30-60min P 6-90mins

Question 17

Neostigmine:
Moa?
Dose?
Onset?

Answer 17

Moa: antagonizes the action of acetyl-cholinesterase leading to an increased amount of Ach accumulating in the synaptic cleft and displacing the non-depolarising neuromuscular blocker from the nicotinic receptor.
Dose: 50mcg/kg
Onset: 6-10mins

Question 18

What does the TOFC and TOFR need to be to give Neostigmine?
What else is given with Neostigmine?
Why?
Dose?

Answer 18

Reversal is required if TOFC <4 with a TOFR of <0.9
Atropine
To reduce the risk of ACh activating muscarinic receptors causing SLUDEM
Dose: 20mcg/kg

Question 19

What are the two drugs given with reversal of NDMR?
Which one is more expensive?
Which one crosses the BBB?

Answer 19

Atropine and Glycopyrrolate
Glyco
Atropine

Question 20

Sux causes fasciculations, what are the side effects of this?

Answer 20

Fasciculations cause patient movement and are more marked in muscular subjects making optimum patient positioning important before giving sux. They have been implicated in sux myalgia- muscle aches usually experienced the following day with physical activity. They are self-limiting.

Question 21

What is cardiogenic complication of sux?
When does this occur?
What age group is more susceptible?
Why?

Answer 21

sux binds to the SA node and can cause a marked
bradycardia.
Occurs: with a second dose of sux
Age: children as they have higher resting vagal tone and so should be given with great caution in this instance or
after pre-treatment with an anticholinergic agent.

Question 22

Describe scoline apnoea
What are the 4 commonest forms? USAF
How is it identified?

Answer 22

Genetically variable forms of abnormal plasma cholinesterase lead to impaired metabolism of sux and consequent prolonged duration of action
Usual Silent Atypical Fluride
Blood test = cholinesterase levels and genetic testing

Question 23

How much is the normal increase in K when using Sux?
Why does this occur?
Why does this occur more in certain conditions? Re: receptors

Answer 23

0.5-1mmol/L
Caused by effluent of K into the ECC by depolarisation of the nicotinic receptors.
This occurs when cholinergic receptors are located outside of the motor end plate or are hypersensitised, causing K efflux elsewhere

Question 24

How long does it take for the risk of hyperkalaemia in burns using sux last?

Answer 24

Up to 18 months

Question 25

``` RECURONIUM Metabolism? Elimination? Diurnal variability? Precipitates with? Histamine release? ```

Answer 25

``` Met = liver Elim = kidney + bile Variation = ~50% longer in morning vs afternoon Precipitates = thiopentone Hist = no ```

Question 26

``` VECURONIUM Dose? Onset? Duration? Maintenance? ```

Answer 26

``` 0.1mg/kg 3min Duration = 20-30mins Maintenance = 1-2mg MOA = competitively antagonising ACh at the post-junctional nicotinic receptor. Binds to alpha unit ```

Question 27

What nicotinic receptor subunits are there? Which one does NDMR bind to? How many do they need to bind to?

Answer 27

``` Alpha x2 Beta Delta Epsilon NDMR bind to the alpha sub unit Only one needs to bind to antagonist receptor ```

Question 28

Describe the mechanism of action of Sux on the voltage-gated channels in the muscle membrane

Answer 28

One channel two gates (M and H) At rest M is shut and H is open Sux causes depolarisation, opening the voltage-dependent M gate. After a short period of time the time-dependent H gate shuts. Instead of a wave of depolarisation resulting in return to resting state the continued depolarising causes H gate to stay shut as it relied on the repolarisation to reset and open again max

Question 29

What is the difference between cholinesterase and acetyl cholinesterase? What does this mean for Sux?

Answer 29

Cholinesterase metabolised Sux before it gets to the synaptic cleft. Acetyl cholinesterase metabolises ACh in the synaptic cleft. This means a large amount of Sux is metabolised before it reaches the target site, requiring a large dose (1mg/kg) to allow it to have an effect

Question 30

What is the priming principle for muscle relaxants? What is the reasoning behind this? What percentage of receptors need to be activated to have twitch height? Intubation?

Answer 30

A small dose of NDMR is given prior to the conventional dose of relaxant in order to shorten the onset of action. The spare receptor concept describes the huge reserve of receptors that need to be activated to have an effect. 75% for twitch height, 95% for intubation.

Question 31

``` NEOSTIGMINE MOA? ‘Convenient’ dose? Max dose? Onset of action? What other drug is given with neostigmine? Why? ```

Answer 31

Antagonises the action of acetyl cholinesterase in the synoptic cleft, increasing the number of ACh which pushes NDMR off of receptor Dose = 1 ampule which is 2.5mg Max = 50mcg/kg Onset - 6-10mins Atropine given to minimise the risk cholinergic overstimulation of the muscarinic receptors.

Question 32

``` ATROPINE Moa? Dose? Ampoule? Onset? Cross Blood brain barrier? ```

Answer 32

``` Anti cholinergic by antagonising muscarinic receptors Dose = 20mcg/kg Ampoule = 1.2mg Onset = 1-2mins Crossed blood brain barrier ```

Question 33

What law dictates how the pulse oximetry works?

Answer 33

``` Beer-Lambert law for absorbance of light A = elc Absorptivity optical length Concentration ```

Question 34

What is the induction dose of propofol? | What is the rate of propofol infusions?

Answer 34

Induction - 2-2.5mg/kg Maintenance - 4-12mg\kg\hr OR 75-175mcg\kg\min

Question 35

What infusion rate and duration is associated with propofol infusion syndrome? What does it look like clinically? Adults or children?

Answer 35

doses of >4mg/kg/hr for >48 hours Clinically - severe metabolic acidosis, bradycardia, multiorgan failure and treatment resistant cardiac arrest (described mainly in children)

Question 36

What will you lose if the power goes out? | Which volatile anaesthetic doesn’t work without power?

Answer 36

Ventilation and monitoring | Desflurane

Question 37

How does a pulse oximetry work?

Answer 37

Measures the relative absorption of light by oxyhaemoglobin (HBO) and deoxyhaemoglobin via measuring the amount of red and infrared light emerging from the tissues over the emitted light