Drugs Flashcards
- How does metaraminol work
- Why do you get a bradycardia?
- Pure alpha 1 receptor agonist leading to peripheral vasoconstriction
- Reflex bradycardia due to increased venous return
Drug dilution for remifentanil
1mg in 20ml 0.9% saline or 5% dextrose to make 50mcg/ml
Or 2mg in 40ml
Name of remifentanil TCI model
What it’s used for
Minto model
- Where does remifentanil work?
- How is is metabolised & why
1.Remifentanil is a pure μ-opioid (Mu-opiod) receptor agonist working at this receptors in CNS and peripheries. It inhibits release of pain-transmitting neurotransmitters (e.g substance P, glutamate)
2. Its structure is similar to fentanyl but has an ester group allowing it to be rapidly metabolised by non specific tissue and plasma esterases
(Safely used in patients with pseudocholinesterase deficiency)
Its major metabolite, remifentanil acid, undergoes renal excretion and accumulates in patients with reduced renal function1,2. Despite this, the dosing of remifentanil does not need to be adjusted for renal dysfunction as remifentanil acid is almost entirely inactive1,2.
Post-operative shivering is twice as likely to occur with remifentanil3.
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- What is the minto model?
- What have the effector site (Cet) constant (keo) & LOC been derived from?
- The Minto model is a three compartment model programmed to target either effector site or plasma site.
- Effector site constant and LOC have been derived from EEGs parameters.
- The increased initial concentration in effect mode is 3-4x greater than in plasma site (Cpt) mode & may be associated with a greater incidence of adverse effects (chest wall rigidity, bradycardia, apnoea)
It is advisable that clinicians unfamiliar with the use of remifentanil TCI use Cpt in preference to Cet.
Is Remifent safe in malignant hyperthermia?
Yes
Is Remifent safe in malignant hyperthermia?
Yes
What effect site concentrations are recommended for remi
4-6ng/ml laryngoscopy & intubation
6-8 painful ops such as laparotomy
10-12 cardiac surgery
Specific indications for TIVA
Malignant hyperthermia risk
Long QT (QTc >500ms)
History of severe PONV
Tubeless ENT or thoracic surgery
Anticipated difficult intubation/ extubation
Neurosurgery (to limit intracranial volume)
Surgery requiring neurophysiological monitoring
Myasthenia Gravis & when NMB would be disadvantage.
Anaesthesia in non theatre environments
Transfer
Daycase
Trainee teaching
Patient choice
Specific indications for TIVA
Malignant hyperthermia risk
Long QT (QTc >500ms)
History of severe PONV
Tubeless ENT or thoracic surgery
Anticipated difficult intubation/ extubation
Neurosurgery (to limit intracranial volume)
Surgery requiring neurophysiological monitoring
Myasthenia Gravis & when NMB would be disadvantage.
Anaesthesia in non theatre environments
Transfer
Daycase
Trainee teaching
Patient choice
which infusion is most likely to cause hyperglycaemia in critical care despite patients not being diabetic.
E.g patients BM is 13 mmol 12 hours after starting infusion- which drug is most likely responsible for this?
adrenaline infusion by stimulating glycogenolysis, gluconeogenesis & lipolysis
why is Alfentanil useful in short procedures compared to fentanyl
Alfentanil has a slower clearance than fentanyl but it’s smaller volume of distribution leads to a shorter half life (1-2hrs, with VoD 4-5L) as opposed to Fentanyls half life (3-8hours, with VoD 300-400L)
Alfentanil is most useful due to it’s smaller VoD meaning it has a faster offset.
Alfentanil has a shorter elimination half life than fentanyl (despite it’s slower clearance) because of the lower VoD
Alfentanil also has a quicker onset due to it’s lower pKa (6.5) meaning a larger proprotion exists in its un-ionized, lipid soluble form at physiological pH
max safe dose of levobupivicaine with and without adrenaline
e.g caudal block in 12.5kg for hernia repair ?volume and percentage
2mg//kg with or without adrenaline
most appropriate to used 10mls of 0.25% as it’s a safe dose and volume likely to spread to cover area required (iliohypogastric, ilioguinal nerves, T11 & T12 intercostal nerves). Using higher conc (0.5%) is more likely to lead to motor weakness, and is not needed.
which metabolite of diamorphine is most likely to cause resp despression on patient with renal failure
increased plasma conc of morphine-6-glucuronide
what is acetazolamide and how does it work
Clinical uses
acetazolamide is a carbonic anhydrase inhibitor that primarily works in PCT.
- Inhibits carbonic anhydrase (CA): Normally, CA converts H₂CO₃ (carbonic acid) → CO₂ + H₂O, allowing for bicarbonate (HCO₃⁻) reabsorption.
- Increased renal bicarbonate excretion:
Blocking this enzyme reduces HCO₃⁻ reabsorption, leading to bicarbonate loss in urine.Causes alkaline urine and decreased blood HCO₃⁻, leading to metabolic acidosis. - Mild natriuresis and diuresis: Na⁺ and water loss occurs, but it’s not a strong diuretic like loop diuretics
CLINICAL USES:
-glaucoma (reduces aqueous humor production)
-to correct metabolic alkalosis through loss of HCO3-
-altitude sickness (induces acidosis, leading to hyperventilation)
-idiopathic intracranial HTN (Reduces CSF production)
SE: hypokalaemia, acidosis -> avoid in renal failure
What drugs must be avoided if patient is on MAOIs e.g selegiline
- Avoid sympathomimetic agents (risk of hypertensive crisis)
e.g avoid ephedrine (can cause extreme hypertension due to excessive norad release), phenylephrine, pseudoephedrine (found in some decongestants)
2.opiods:
-pethidine (can cause serotonin syndrome)
-tramadol- risk of serotonin syndrome
-fentanyl, alfentanil -may have unpredictable results.
Safer alternatives-> remifent, morphine
- induction agents
-caution with ketamine (risk of excessive sympathetic stimulation
-thiopental-may cause exaggerated CNS depression.. - LA- risk of hypertensive crisis if used with adrenaline.
- muscle relaxants- sux-> risk of prolongation if pseudocholinesterases are depleted.
IDEALLY STOP 2/52 prior to surgery.
ESPECIALLY IF IRREVERSIBLE MAOI like selegiline
other examples of MAOIs:
-irreversible non selective MAO-A and MAO-B inhibitors (HIGH RISK OF HYPERTENSIVE CRISIS)- phenelzine, tranylcypromine, isocarboxazid (these are older generate used for depression and PD.
-irreversible selective (MAO-B only)- primary used for PD to prevent breakdown of dopamine- Selegiline, Rasagiline.
-> risk of interactions with pethidine, SSRIs, ephedrine
-Reversible MAO-A inhibitors-> moclobemid used in depression, less risk of hypertensive crisis
what is the reversal of unfractionated heparin
reversal in massive bleeding/ emergency surgery:
-protamine sulfate IV
-consider FFP or Prothrombin complex concentrate
-TXA may be used to support clot formation
if protamine is contraindicated (allergy to fish derived products)-> stop heparin, supportive care (blood products, FFP)
in the context of burns, when should sux be avoided and why
avoid if >24hours post burn due to upregulation/ increased formation of extrajunctional ACh receptors which can cause massive potassium efflux , thus resulting in hyperkalaemia.
-normal K rise after potassium: around 0.5mmol/L
-in burns this can be >5-10mmol-> risk fo cardiac arrhythmia and arrest
what is Nimodipine and what is it commonly used for
Nimodipine is a CCB used in SAH to reduce vasospasm which could lead to further neurological damage or stroke.
risk of delayed cerebral ischaemia is significant in patients with SAH.
Nimodipine has high affinity for cerebral tissue
SE: hypotension, bradycardia, headache, nausea & dizziness, electrolyte imbalance
PO 60mg 4hourly starting withiin 96 hours of SAH and continuing for 21 days
IV dose? unsure
