Neurological Flashcards
Levetiracetam (keppra)
Anticonvulsant
Dose- 500mg BD
Use: partial onset seizures, generalised tonic/clinic seizures, status epilepticus
Inhibit burst firing without affecting normal neuronal excitability and May selectively prevent hypersynchronisation of epileptiform burst firing and propagation of seizure activity
Nursing responsibility- assess for fatigue, coordination and behavioural issues, assess for suicidal thoughts, assess for rash, monitor FBE
Contraindicated- hypersensitivity
Cautiously- increases risk suicidal thoughts, renal impairment
Adverse effects- CNS- suicidal thoughts, aggression, agitation, anger, apathy, co-ordination difficulties, depersonalisation, depression, dizziness, drowsiness, fatigue, hostility, irritability, personality disorder, psychosis, weakness, hyperkinesia
CVS- hypertension
Skin- drug reaction with eosinophilia and systemic response (DRESS), Stevens Johnson’s syndrome, toxic epidermal necrolysis
Haem- agranulocytosis, anaemia, eosinophilia, neutropenia, thrombocytopenia,
General anaesthetic
Higher cortical functions (conscious thought, memory, motor control, perception of sensation) suppressed first then medullary centres (cardiovascular and resp control)
Four stages of GA
1- analgesia- onset=loss of consciousness. Sense of pain and smell go first then vivid dreams and auditory/visual hallucinations, numbness spreads gradually, hearing is last to go
2- excitement- varies with individual and meds. Reflexes still present or exaggerated, swallowing reflex abolished. Autonomic activity, eye movement, pupil dilation and rapid breathing increase, vomiting/incontinence may occur
3- surgical anaesthesia- divides into 4 planes of depth
4- medullary paralysis (toxic stage)- impending overdose, resp arrest, vasomotor collapse
GA’s decrease functions of excitatory neurotransmitters (acethycholine, 5-HT, glutamate, NMDA), increasing function of inhibitory neurotransmitters (GABA and glycine)
Inhalation GA (gases and volatile liquids)- nitrous oxide, sevoflurane, methoxyflurane (green whistle)
IV GA’s-
-ultra short acting barbiturates (thiopental-depresses reticular activating system). Adverse effects=shivering, trembling, nausea, vomiting, headache, delirium, cardiac dysrhythmias, resp depression, bronchospasm
-non-barbiturates (propofol, ketamine, benzodiazepam). Rapid action as high lipid solubility, short duration as redistributed into fat deposits of body. Adverse effects=resp, reflex and cardiovascular depression, post op convulsions, headache, nausea, vomiting, kidney and liver toxicity, malignant hyperthermia, hypersensitive reactions, neurotoxicity
Depolarising neuromuscular blockers- (suxamethonium-muscle relaxant)- activate acetylcholine receptors at the neuromuscular junctions, enhances by anticholinergics
Non-depolarising neuromuscular blockers (pancuronium-skeletal muscle paralysis)- competitive antagonist of acetylcholine at neuromuscular junctions. Reversible with anticholinergics
Local anaesthetic
Reversibly prevent the generation of impulses in excitable membranes and decrease sensitivity to pain
The non-ionised form enters the cell by diffusion through the membrane where it becomes ionised and binds to a modulatory site in the voltage dependant sodium channel blocking the sodium channel and interfering with the opening of the channel which prevents the threshold from being reached thus no depolarisation or action potential and thus blocks nerve
Cause vasodilation by direct action on blood vessels and anaesthetising sympathetic vasoconstrictor fibres, causes rapid absorption into sympathetic system. Vasoconstrictors such as adrenaline can be added to local anaesthetic to reduce systemic absorption
Adverse reaction- local inflammation, psychogenic reactions (syncope, vasovagal), sympathetic stimulation, hypotension, headache, parasthesia, allergies, numbness of tongue, tremor, irritability, CNS depression, relaxation of smooth muscle, cardiovascular and resp depression
Phentolamine (a blocker) dilates vessels at injection site and allows faster clearance of local anaesthetic
Benzodiazepams
Anti anxiety, muscle relaxant, antiepileptic, hypnotic, memory-impairing
Works by binding to GABA receptors which are ligand-gated chloride channels. When activated there is increased chloride permeability and influx of chloride into the cell causing hyperpolarisation and decrease excitability of the neuron
Lipid soluble and readily absorbed from GI tract
Redistribution from CNS to peripheral can reduce duration of action
Metabolised by liver and GI
Anxiety, withdrawal & muscle spasm=diazepam
Sleep=temazepam
Seizure=midazolam/clonazepam.
Status epilepticus=parenteral diazepam
Adverse reactions- CNS depression, drowsiness, ataxia, diplopia, vertigo, memory loss, slurred speech, loss of dexterity, headaches, loss of libido, antegrade amnesia, muscle weakness, hypotension, insomnia, hallucinations, increased excitability
Management of adverse reactions- maintain airway, O2, monitor vitals, promote diuresis with IV fluids, flumazenil IV (Benzo reversal), May need to be repeated due to long life of benzos
Antiepileptic
Phenytoin, carbamazepine, sodium valproate, lamotirgine
Barbiturates (phenobarbitone)- non selective depression of the CNS via facilitation of chloride entry into cells at GABA receptors and enhance inhibitory systems that use GABA as a neurotransmitter
Adverse reactions- sedation, ataxia, confusion, depression of cardiovascular and resp centres, impaired memory, can enhance Vit D metabolism and cause reduced bone mineral density
Vigabatrin- enhances GABA mediated inhibition through irreversible inhibition of GABA transaminase (enzyme that inactivates GABA)
Thiagabline and topiramate- adjunctive therapy in seizures not well controlled by other meds
Phenytoin- blocks voltage dependant sodium channels decreasing propagation of seizures. Not to be used with enteral feeds 2hrs either side
Carbamazepine- blocks sodium channels preventing repetitive neuronal discharges and decreasing seizures. Oral absorption is slow and may take months to reach therapeutic levels. Not with grapefruit.
Sodium valproate- enhanced brain GABA levels and block sodium, potassium and calcium channels. Works through competitive inhibition and prevents reuptake of GABA. Food delays absorption- metabolised in GI
Lamotrigine- blocks sodium channels and inhibits release of excitatory neurotransmitter (glutamate and aspartate)
Ketamine
0.1-0.3mg/kg/hr
Usual dose range 7-24mg/hr
Infusion rate 1.75-6ml/hr
Prep- 200mg(2ml) made up to 50ml of N/S or glucose 5%
4mg/ml= 4mg/hr
Needs co-infusion
NMDA receptor antagonist
Metabolised in kidneys
Half life 2-3hours
Contraindications- uncontrolled heart failure, uncontrolled hypertension, AMI, acute psychotic states, methamphetamine use, TBI
Side effects- increased saliva, hallucinations, confusion, excitement, irrational behaviour, insomnia, hypertension, tachycardia, increased intra-ocular pressure, muscle hyperactivity, laryngospasm, resp depression
Obs- 1/24 first 4/24, 2/24 for next 4/24 then 4/24 after
Midazolam
300mg in 250mls N/S =1mg/ml
Dose range 1-10mg/hr
Or
100mg in 100ml (remove 20ml)
1mg/ml=1mg/hr
Bind to GABA receptors
Depresses subcorticol levels in CNS
Sedation, antiepileptic, anxiety
Side effects- resp depression, apnoea, hypotension, paradoxical agitation
Cistacurium
Loading dose 0.15mg/kg over 30sec
Dose range 1-20mg/hr
Infusion- 50mg (25mls) made up to 50mls N/S
1mg/ml
Elimination half life 22-29mins
Non-depolarising benzylisoguiotinium
Neuromuscular blocking agent
Binds to cholinergic nicotinic receptors on end plate to antagonise action of acetylcholine resulting in competitive block of neuromuscular transmission
Titrate to train of 4 1-2
Side effects- prolonged recovery, bronchospasm, rash, bradycardia, hypotension
Nursing consideration- monitor paralysis, continuous monitoring, CO2 monitoring, monitor neurological status
Clonidine
Prep- 900mcg in 100mls (remove 16ml) of N/S
10mcg/ml
25mcg/hr increase every 30min to effect
Wean by 25-50mg/hr
Dose range 50-200mcg/hr
Convert 1:1 IV to oral
Centrally acting alpha Adrenoreceptor agonist of postsynaptic receptors (blocking uptake)
Reduces sympathetic drive, decreased peripheral resistance, decreased renal vascular resistance, reduced blood pressure and HR
Uses- drug withdrawal, delirious or agitated patient
Side effects- hypotension, bradycardia, rebound hypertension, dizzy, nausea, drowsy, parasthesia
Nurse consider- continuous monitoring, RASS monitoring, delirium scores
Fentanyl
Prep- 3000mcg (50mls) in 250ml N/S
10mcg/ml
Or
1000mcg in 100ml=10cg/ml
Remove 20mls
Loading dose 1-3mcg/kg
Dose range 10-150mcg/hr- 1-15ml/hr
Inhibits ascending pathways in CNS, binding to opioid receptors, increased pain threshold, reduced pain perception
Side effects- resp depression, bradycardia, muscular rigidity
Monitor CNS changes
Dexametimidine
0.7mcg/kg/hr
Dose range 0.2-1.5mcg/kg/hr
Max 100kg weight
Max duration 48hrs
Titrate 0.1-0.2mcg/kg/hr every 30mins-2hrs
Prep- 1000mcg (5 vials=10mls) in 100mls N/S or glucose 5% (remove 10mls)
10mcg/ml
Thiopentoine
Bolus 500mg vial in 20ml water give slowly
Infusion- 5g (reconstituted 200ml) in 500ml N/S or glucose 5% (remove 200ml)
10mg/ml
10ml/hr
Propofol
Short acting interacts with GABA receptors, produces vasodilation due to reduced catecholamines circulating
-Can reduce ICP and seizures
-Metabolised by liver
- contraindications- egg/soybean/glycerol allergy,
- change line every 12hrs
- bolus doses 0.1-1mg/kg
-infusion up to 2mg/kg/hr
Concentration = 10mg/ml
Ok to be infused with midaz, fentanyl, morphine, dexmed
Side effects- hypotension, bradycardia, pain at injection site, Propofol infusion syndrome (metabolic acidosis, hyperkalaemia, lipaemia, rhabdomyolosis, dysrhythmia)
Paracetamol
Non opioid analgesic
Antipyretic
Block pain responsible peripherally due to Inhibition of prostaglandins
Inhibition of prostaglandins in CNS (hypothalamic-heat regulating centre)
Side effects- N&V, rash, neutropenia, hepatotoxicity, LFT + renal functions
