Drugs Flashcards
How do inhaled aesthetics work?
Not entirely sure, however though to be due to modulation of GABA in brain and glycine in spinal cord
Nitrous Oxide
- Rapid onset, low potency
- adverse effects
Dont use it very often but can be used in combination with other drugs
Entonox - 50% oxygen - maternity, for wound dressings - euphoric effect - laughing gas
-non addicctifvae
Sevoflurane, Isoflurane, Desflurane
Sevoflurane - easy inhaled - used for children
Isoflurane - Good CV stability - used in these surgeries
Desflurane - Rapid onset and offset - good for long cases
Mechanism of action of IV anesthetics
-Enhanced action of GABA receptor in brain, leads to enhanced action of inhibitory neurons (so enhanced inhibition of excitatory neurons)
Ketamine - works in a different way - binds to excitatory receptors in spinal cord (blocks excitatory synapses)
Highly lipid soluble
- crosess BBB easily
- redistributes to many places in body
Thiopentone
Propofol
Etomidate
Ketamine
LEARN WELL
Thiopentone - Use when want patient to sleep fast e.g ceserian section
- Cannot keep patient asleep with this (slow clearance)
- CV instability
- Resp depression and loss of airway reflexes
Propofol
- General use - no hangover (rapid onset, fast clearance)
- good in nuerosurgery
- CV instability
- Resp depression and loss of airway reflexes
- Very narrow therapeutic index
Etomidate
- CV stability - use for coronary disease
- less respiratory depression
Ketamine
- Good for shock patients (increases CO, preserves airway reflexes and resp drive)
- analgesic (other ones dont have this)
- has euphoric effect - can get addiction
IV vs Gas
IV - avoids inhalation complications
- cannot measure
- Expensive
How do local anaesthetics work?
Block sodium channels at nerve endings - prevents sodium entering cell and blocks nuerotransmission
Weak bases - non-ionised form can enter cell membrane and then ionize again in cells to block sodium channels
-Faster onset of action with more free base present, and also those with a pKA closer to body pH
Local anesthetics
Potency
Duration
Onset of action
What do these reflect?
Potency level - depends on how lipid soluble molecule is - more lipid soluble - more potent
Protein binding - increase this, than increase duration of aciton
Ionisation - more free base present - faster onset of action (lower pKA - more free base)
liognocaine, Bupivacaine, cocaine, prilocaine, ropivacaine
Toxicity
Lignocaine - standard that we compare others to
- Low potency, low protein binding, fast onset (low lipid solubility, highly non-ionized, low protein binding)
- Ideal for short surgical procedures e.g dental or mole removal
Bupivacaine
- higher lipid solubility, pka and protein binding
- Ideal for nerve blocks for analgesia
Cocaine
- topical use - vasoconstriciton - can limit bleeding
- Potent inhibitor of catecholamine re-uptake
Prilocaine
- Safest agent
- can put limb to sleep without rest of body
Ropivacaine - similar to bupicaine, long acting, less cadiac toxicty
Toxicity - first get Cardiac toxicity than cns toxicity. Ratio - shows how safe it is
-seizure is the first sign that overdose
What can you used for topical , soft tissue infiltration
Topical - EMLA - lignocaine and prilocaine in oil preparation - allows most base to move across skin - good for insertion of IV cannulae in children
Topical - mucous membranes - cocaine, lignocaine spray - e.g to get tube down patient
Soft tissue infiltration
-lignocaine - fast actign, short duration e.g dentist procedures
For post opperative pain relief - want slow acting, long duration e.g bupivacaine ?
When to use nerve blocks - peripheral, spinal nerve, epidural
Can do it in spinal cord or in peripheral nerve
Spinal nerve - inject into intrathecal space below L2 (this is where spinal cord terminates)
- distal motor and sensory blockade - fully numb
e. g hip replacement, Caesarean section if not urgent
Peripheral - with local anesthetics around a nerve, used for surgeries without anaesthetic, or post op pain relief
Epidural - catheter into epidural space -can be done at any level -distal sensory and motor blockade -excellent post op labour analgesia
Why use neuromuscular blocking agents?
-Paralyse patients for surgery, or for ventilation - put tube down throat will not get reflexes or cause pain to patient , used in emergency conditions
Depolarising NMBA
side effects
whats used for
Succinylcholine - depolarising NMBA -
- agonist, binds to ACHR, will not unbind so cannot get repolarisaiton
- fast onset of action, short duration of action
- broken down and has a short half life
SUCCINYLCHOLINE APNOAE - cannot be reversed by drugs, can get toxicity, paralysis
-broken down by accetylcholine esterase
Non-depolarising NMBA
How to reverse
- bind to ACHR subunit and prevent opening of the channel - no depolarisation
- e.g Rocuronium
- low potency, rapid onset of action
- longer duration
How to reverse
- give perfect dose
- increase the ACH conc (inhibit its breakdown in cleft - outcompetes drug - anticholinesterase)
- decrease plasma conc of it at NMBA (sugammadex - binds to rocuronium in plamsa, decreases amount there - quick return of muscular function)
How to monitor neuromuscular blockade
- Electrically stimulate peripheral nerve and see muscle response
- Train of 4 - if get fade of twitch than not worn off yet
