p.9
Neuromuscular Blocking Drugs Classification and Mechanism
What type of muscle relaxant is Pancuronium bromide?
Aminosteroid non-depolarising muscle relaxant.
p.12
Physiochemical Properties of Volatile Agents
What is the concentration of Mivacurium in its solution?
2 mg/mL in 5 and 10 mL vials.
p.25
Mechanisms of Action of Inhalational Anaesthetics
How do opioids exert their effects?
Opioids stimulate presynaptic G-protein-coupled opioid receptors, leading to closure of voltage-gated Ca2+ channels, decreased cAMP production, K+ efflux, hyperpolarization of the cell membrane, decreased excitability, and reduced neurotransmitter release and pain transmission.
p.13
Mechanisms of Action of Inhalational Anaesthetics
How does Vecuronium Bromide bind to the nicotinic receptor?
It binds to the α-subunit but does not stimulate it to open the ion channel.
p.25
Opioid Pharmacology and Effects
What effect does morphine have on its receptors?
Morphine seems to cause uncoupling of its receptors but not down-regulation.
p.17
Anticholinesterase Agents and Their Uses
What is the primary use of Neostigmine?
Reversal of neuromuscular blockade caused by non-depolarising muscle relaxants.
p.13
Mechanisms of Action of Inhalational Anaesthetics
What is the mechanism of action of Vecuronium Bromide?
Competitive inhibition of ACh at nicotinic receptors at the neuromuscular junction.
p.21
Anticholinesterase Agents and Their Uses
What type of amine are hyoscine and atropine?
They are tertiary amines.
p.12
Neuromuscular Blocking Drugs Classification and Mechanism
What type of muscle relaxant is Mivacurium?
A benzylisoquinolinium non-depolarising muscle relaxant.
p.13
Neuromuscular Blocking Drugs Classification and Mechanism
How long does the effect of Vecuronium Bromide last?
Approximately 45 minutes.
p.15
Anticholinesterase Agents and Their Uses
What are the classifications of anticholinesterases based on duration of action?
Short acting, medium acting, and long acting.
p.8
Neuromuscular Blocking Drugs Classification and Mechanism
How quickly can sugammadex terminate the effects of rocuronium?
In 1.5 minutes when given 3 minutes after an intubating dose.
p.25
Opioid Pharmacology and Effects
What is the difference between an opiate and an opioid?
Opiates are naturally occurring compounds derived from opium (e.g., morphine, codeine), while opioids are synthetic substances that stimulate opioid receptors (e.g., fentanyl, alfentanil).
p.23
Mechanisms of Action of Inhalational Anaesthetics
What is the mechanism of action (MOA) of Atropine?
It acts as a competitive antagonist at muscarinic receptors ('vagolytic').
p.2
Physiochemical Properties of Volatile Agents
What is the structure of most inhalational agents?
Most are halogenated ethers, except halothane and nitrous oxide.
p.17
Cardiovascular Effects of Inhalational Agents
What are some cardiovascular effects of Neostigmine?
Bradycardia and hypotension.
p.1
Factors Affecting Speed of Onset of Anaesthesia
How does high inspired concentration (F i) affect the delivery of anesthetic?
It increases the delivery of the drug to the alveolus and leads to a more rapid rise in alveolar partial pressure (P a).
p.24
Anticholinesterase Agents and Their Uses
What are some uses of Glycopyrrolate?
To decrease oral secretions, attenuate effects of anticholinesterases, treat bradycardia, and manage hyperhidrosis.
p.15
Anticholinesterase Agents and Their Uses
How do anticholinesterases exert their effects?
They inhibit the action of acetylcholinesterase by occupying its active site, preventing it from breaking down acetylcholine.
p.13
Neuromuscular Blocking Drugs Classification and Mechanism
What type of muscle relaxant is Vecuronium Bromide?
Aminosteroid non-depolarising muscle relaxant.
p.17
Mechanisms of Action of Inhalational Anaesthetics
What is the mechanism of action (MOA) of Neostigmine?
Binds to the esteratic site of acetylcholinesterase (AChE), increasing the availability of acetylcholine (ACh) at the neuromuscular junction.
p.6
Mechanisms of Action of Inhalational Anaesthetics
What happens when acetylcholine binds to the nAChR?
The receptor undergoes a conformational change, opening the central pore for ion flow.
p.8
Neuromuscular Blocking Drugs Classification and Mechanism
What was the primary class of drugs used to reverse non-depolarising neuromuscular blockers until recently?
Anticholinesterases, such as neostigmine.
p.5
Minimum Alveolar Concentration (MAC)
What factors have no influence on Minimum Alveolar Concentration (MAC)?
Duration of anaesthesia, gender, alkalosis, hypertension, anaemia, magnesium and potassium levels.
p.24
Anticholinesterase Agents and Their Uses
What type of drug is Glycopyrrolate?
A synthetic quaternary amine.
p.8
Neuromuscular Blocking Drugs Classification and Mechanism
How do anticholinesterases work?
By increasing the concentration of acetylcholine at the neuromuscular junction.
p.17
Metabolism and Toxicity of Inhalational Anaesthetics
How is Neostigmine metabolized?
Metabolised by plasma esterases with some hepatic metabolism; excreted in bile and urine.
p.4
Cardiovascular Effects of Inhalational Agents
How does sevoflurane affect heart rate (HR)?
Sevoflurane decreases heart rate (↓).
p.4
Cardiovascular Effects of Inhalational Agents
What is the effect of desflurane on cardiac output (CO)?
Desflurane has no significant effect on cardiac output (↔).
p.22
Metabolism and Toxicity of Inhalational Anaesthetics
What is the major cause of side effects from these pharmacological agents?
Their antagonistic action on the 'rest and digest' activity of glands, smooth muscle, and cardiac muscle.
p.15
Anticholinesterase Agents and Their Uses
What is the mode of action of neostigmine?
It carbamylates the active site of acetylcholinesterase, prolonging the effects of acetylcholine.
p.6
Neuromuscular Blocking Drugs Classification and Mechanism
What is the structure of the nicotinic acetylcholine receptor (nAChR)?
It is composed of five subunits: two α, one β, one δ, and one γ, arranged around a central pore.
p.15
Anticholinesterase Agents and Their Uses
What is the primary use of anticholinesterases?
To reverse the effects of non-depolarising neuromuscular blocking drugs by increasing the amount of acetylcholine available.
p.25
Opioid Pharmacology and Effects
What are the four main types of opioid receptors?
μ receptor (subtypes μ1, μ2, μ3), κ receptor (subtypes κ1, κ2, κ3), δ receptor (subtypes δ1, δ2), and NoP receptor (nociceptin orphanin FQ peptide receptor).
p.14
Neuromuscular Blocking Drugs Classification and Mechanism
What type of muscle relaxant is Rocuronium bromide?
Aminosteroid non-depolarising muscle relaxant.
p.21
Anticholinesterase Agents and Their Uses
What is the structure of glycopyrrolate?
It is a synthetic quaternary amine.
p.1
Comparison of Isoflurane and Sevoflurane
Which agent has a faster onset of anesthesia, isoflurane or sevoflurane?
Sevoflurane has a faster onset of anesthesia.
p.21
Anticholinesterase Agents and Their Uses
Which drug can cross the blood-brain barrier (BBB)?
Hyoscine and atropine can cross the BBB; glycopyrrolate cannot.
p.8
Physiochemical Properties of Volatile Agents
Why do aminosteroidal neuromuscular blockers have a low volume of distribution?
Because they are bulky and polar, making it difficult for them to cross cell membranes.
p.24
Metabolism and Toxicity of Inhalational Anaesthetics
How is Glycopyrrolate metabolized and excreted?
Minimal metabolism; excreted unchanged in urine.
p.17
Cardiovascular Effects of Inhalational Agents
What are the central nervous system effects of Neostigmine?
Miosis, blurred vision, and muscle contraction at low doses; potential neuromuscular transmission blockage at high doses.
p.15
Anticholinesterase Agents and Their Uses
What is a common use for neostigmine?
Reversal of competitive neuromuscular blocking drugs and treatment of constipation in the ICU.
p.2
Metabolism and Toxicity of Inhalational Anaesthetics
How does nitrous oxide affect vitamin B12?
It oxidizes the cobalt atom in vitamin B12, leading to bone marrow depression.
p.23
Metabolism and Toxicity of Inhalational Anaesthetics
What are some common side effects of Atropine?
Dry mouth, urinary retention, and blurred vision.
p.1
Factors Affecting Speed of Onset of Anaesthesia
What is the concentration effect in relation to nitrous oxide (N2O)?
The concentration effect occurs when N2O is used in high concentration, leading to a disproportionate rise in alveolar partial pressures of other gases.
p.3
Mechanisms of Action of Inhalational Anaesthetics
How does Nitrous Oxide affect the NMDA receptor?
It strongly inhibits the NMDA receptor.
p.24
Physiochemical Properties of Volatile Agents
What gastrointestinal effect does Glycopyrrolate have?
Antisialagogue (reduces saliva production).
p.20
Anticholinesterase Agents and Their Uses
What are some uses of hyoscine as an antiemetic?
To treat motion sickness, post-operative nausea, and opioid-induced nausea.
p.20
Anticholinesterase Agents and Their Uses
What is the role of antimuscarinic agents in gastrointestinal procedures?
They are used to facilitate upper gastrointestinal endoscopy.
p.7
Minimum Alveolar Concentration (MAC)
What are ED50 and ED95 in the context of neuromuscular blocking agents?
ED50 is the dose required for 50% depression in twitch height, and ED95 is for 95% depression.
p.19
Anticholinesterase Agents and Their Uses
Does Sugammadex have an affinity for pancuronium?
Yes, but it is not licensed for its reversal.
p.11
Neuromuscular Blocking Drugs Classification and Mechanism
What type of muscle relaxant is Atracurium?
A benzylisoquinolinium non-depolarising muscle relaxant.
p.1
Physiochemical Properties of Volatile Agents
How does the blood:gas coefficient of sevoflurane compare to that of isoflurane?
Sevoflurane has a lower blood:gas coefficient of 0.6, making it less soluble in blood than isoflurane.
p.12
Mechanisms of Action of Inhalational Anaesthetics
What is the mechanism of action of Mivacurium?
Competitive inhibition of ACh at nicotinic receptors at the neuromuscular junction.
p.3
Mechanisms of Action of Inhalational Anaesthetics
What does the Meyer-Overton hypothesis link?
Lipid solubility (oil:gas coefficient) and potency (MAC).
p.1
Factors Affecting Speed of Onset of Anaesthesia
What factors affect the speed of onset of anesthesia with volatile agents?
Inspired concentration, alveolar minute ventilation, functional residual capacity, cardiac output, and the concentration and second gas effect.
p.23
Neuromuscular Blocking Drugs Classification and Mechanism
What are some common uses of Atropine?
To decrease secretions, treat bradycardia, and organophosphate poisoning.
p.1
Factors Affecting Speed of Onset of Anaesthesia
What is the effect of functional residual capacity (FRC) on the onset of anesthesia?
A large FRC dilutes the inspired concentration, resulting in a slower rise in P a and slower onset, while a small FRC leads to a rapid rise in P a and faster onset.
p.4
Cardiovascular Effects of Inhalational Agents
What is the effect of isoflurane on myocardial work and oxygen consumption?
Isoflurane decreases myocardial work and oxygen consumption.
p.20
Anticholinesterase Agents and Their Uses
How does hyoscine differ in its formulations?
Hyoscine hydrobromide crosses the blood-brain barrier, while hyoscine butylbromide does not.
p.4
Minimum Alveolar Concentration (MAC)
What is the MAC required for intubation?
1.3 MAC is required to prevent coughing and movement during endotracheal intubation.
p.2
Metabolism and Toxicity of Inhalational Anaesthetics
What is halothane hepatitis and its risk factors?
It can manifest as reversible transaminitis or fulminant hepatitis, with risk factors including repeated exposure, female sex, obesity, and middle age.
p.10
Metabolism and Toxicity of Inhalational Anaesthetics
What are some potential effects of Suxamethonium?
Arrhythmias, anaphylaxis, malignant hyperpyrexia, hyperkalaemia, myalgia, increased intraocular pressure, and prolonged neuromuscular blockade.
p.7
Neuromuscular Blocking Drugs Classification and Mechanism
How are non-depolarising neuromuscular blocking drugs classified?
They are classified into two groups: Aminosteroids (e.g., vecuronium, rocuronium, pancuronium) and Benzylisoquinolinium esters (e.g., atracurium, mivacurium).
p.7
Factors Affecting Speed of Onset of Anaesthesia
What factors affect the speed of onset of non-depolarising muscle relaxants?
Their bulky structures and relative polarity lead to small volumes of distribution, and their speed of onset is governed by the concentration gradient between plasma and effect site.
p.16
Metabolism and Toxicity of Inhalational Anaesthetics
What is the effect of toxic doses of anticholinesterases?
Can cause sludge syndrome and death by paralysis of the respiratory muscles.
p.9
Mechanisms of Action of Inhalational Anaesthetics
What is the mechanism of action of Pancuronium bromide?
Competitive inhibition of ACh at nicotinic receptors at the neuromuscular junction.
p.3
Metabolism and Toxicity of Inhalational Anaesthetics
What are the metabolites of Halothane?
Trifluoroacetic acid, chloride and bromide ions.
p.8
Mechanisms of Action of Inhalational Anaesthetics
What structural feature of atracurium leads to its breakdown?
An oxygen atom that destabilizes bonds between constituent atoms, leading to Hoffman degradation.
p.10
Mechanisms of Action of Inhalational Anaesthetics
What is the mechanism of action of Suxamethonium?
Binds to α-subunit of nicotinic receptors at the neuromuscular junction, causing chaotic depolarization and fasciculation before flaccid paralysis.
p.2
Metabolism and Toxicity of Inhalational Anaesthetics
What is compound A and its potential toxicity?
Compound A can be produced from sevoflurane reacting with CO2 absorbents, but concentrations are usually below toxic thresholds.
p.26
Opioid Pharmacology and Effects
What are common symptoms of opioid withdrawal?
Anxiety, adrenergic hyperactivity, malaise, abdominal cramps, sweating, and yawning.
p.4
Factors Affecting Speed of Onset of Anaesthesia
How does age affect MAC?
Young age (infants and children) increases MAC.
p.22
Metabolism and Toxicity of Inhalational Anaesthetics
What gastrointestinal side effects can result from these agents?
Decreased bowel movement, paralytic ileus, and reduced lower esophageal sphincter pressure, risking exacerbation of reflux.
p.14
Neuromuscular Blocking Drugs Classification and Mechanism
What is a key characteristic of Rocuronium bromide compared to Vecuronium?
It is 7 times less potent than Vecuronium.
p.19
Anticholinesterase Agents and Their Uses
What are the recommended doses of Sugammadex for moderate and deep neuromuscular block?
2 mg/kg for moderate block and 4 mg/kg for deep block.
p.16
Anticholinesterase Agents and Their Uses
What is the mode of action for Echothiophate?
Phosphorylation of the active site of the enzyme.
p.16
Neuromuscular Blocking Drugs Classification and Mechanism
What are the cardiovascular side effects of neostigmine?
Bradycardia and hypotension.
p.4
Cardiovascular Effects of Inhalational Agents
What is the effect of isoflurane on systemic vascular resistance (SVR)?
Isoflurane causes a significant decrease (↓↓) in SVR.
p.10
Neuromuscular Blocking Drugs Classification and Mechanism
What is Suxamethonium also known as?
Succinylcholine or scoline.
p.6
Neuromuscular Blocking Drugs Classification and Mechanism
How does suxamethonium exert its effects?
It binds to the α subunit of the nAChR, causing depolarization and muscle fasciculations.
p.6
Neuromuscular Blocking Drugs Classification and Mechanism
Why does suxamethonium have a prolonged effect compared to acetylcholine?
It is not broken down by acetylcholine esterase, leading to sustained depolarization.
p.14
Neuromuscular Blocking Drugs Classification and Mechanism
What is the recommended dose of Rocuronium bromide for intubation?
0.6 mg/kg allows intubation in 90–120 seconds.
p.4
Minimum Alveolar Concentration (MAC)
What does MAC stand for in anesthesiology?
Minimum Alveolar Concentration.
p.18
Anticholinesterase Agents and Their Uses
What is the primary use of Edrophonium?
Reversal of neuromuscular blockade caused by non-depolarising muscle relaxants.
p.11
Cardiovascular Effects of Inhalational Agents
What is a potential side effect of Atracurium related to histamine?
It can cause histamine release, leading to hypotension and bronchospasm.
p.18
Mechanisms of Action of Inhalational Anaesthetics
What is the mechanism of action of Edrophonium?
Binds reversibly to the esteratic site of acetylcholinesterase, reducing the breakdown of acetylcholine.
p.11
Factors Affecting Speed of Onset of Anaesthesia
Why is Atracurium useful in patients with renal and liver disease?
Because it is not reliant on these organs for metabolism.
p.18
Anticholinesterase Agents and Their Uses
What is the dose for the Tensilon test using Edrophonium?
2 mg followed by 8 mg if no improvement in strength.
p.26
Opioid Pharmacology and Effects
What is the difference between dependence and addiction?
Dependence is the physical need for a drug to avoid withdrawal symptoms, while addiction involves compulsive drug-seeking behavior despite harm.
p.22
Metabolism and Toxicity of Inhalational Anaesthetics
What respiratory side effect is associated with these agents?
Increased anatomical dead space.
p.19
Anticholinesterase Agents and Their Uses
What is Sugammadex used for?
Reversal of neuromuscular blockade caused by rocuronium and vecuronium.
p.4
Minimum Alveolar Concentration (MAC)
What is the relationship between MAC and inhalational agents administered simultaneously?
MAC is additive when inhalational agents are administered simultaneously.
p.2
Metabolism and Toxicity of Inhalational Anaesthetics
What are the effects of the carbon–halogen bond in inhalational agents?
The bond releases halogen ions, which can be nephrotoxic.
p.7
Neuromuscular Blocking Drugs Classification and Mechanism
What is the minimum receptor occupancy required for clinical effect of neuromuscular blocking drugs?
At least 70% of all receptors must be occupied.
p.7
Factors Affecting Speed of Onset of Anaesthesia
How does the potency of rocuronium compare to vecuronium?
Rocuronium is less potent than vecuronium, requiring a higher dose to achieve the same degree of muscle relaxation.
p.7
Metabolism and Toxicity of Inhalational Anaesthetics
How does liver and renal impairment affect aminosteroids?
It can lead to accumulation of the drugs and prolong their effects.
p.16
Neuromuscular Blocking Drugs Classification and Mechanism
What are the neurological side effects of neostigmine?
Miosis, blurred vision, muscle contraction at low doses, and neuromuscular transmission issues at high doses.
p.11
Mechanisms of Action of Inhalational Anaesthetics
What is the mechanism of action of Atracurium?
Competitive inhibition of ACh at nicotinic receptors at the neuromuscular junction.
p.13
Metabolism and Toxicity of Inhalational Anaesthetics
What is the primary route of metabolism for Vecuronium Bromide?
Hepatic metabolism by deacetylation.
p.24
Mechanisms of Action of Inhalational Anaesthetics
What is the mechanism of action (MOA) of Glycopyrrolate?
It is a competitive antagonist at muscarinic receptors ('vagolytic').
p.23
Metabolism and Toxicity of Inhalational Anaesthetics
How is Atropine metabolized?
Through hepatic metabolism.
p.20
Anticholinesterase Agents and Their Uses
What are antimuscarinic drugs?
Competitive antagonists of acetylcholine at muscarinic acetylcholine receptors.
p.6
Neuromuscular Blocking Drugs Classification and Mechanism
What are some characteristics of an ideal neuromuscular blocker?
Cheap, long shelf life, water-soluble, painless on injection, ultra-rapid onset, predictable duration, and no accumulation.
p.20
Mechanisms of Action of Inhalational Anaesthetics
What is the primary function of antimuscarinic agents?
They reduce the activity of the parasympathetic nervous system.
p.3
Mechanisms of Action of Inhalational Anaesthetics
Which neurotransmitter's breakdown is inhibited by volatile agents?
Gamma amino butyric acid (GABA).
p.10
Metabolism and Toxicity of Inhalational Anaesthetics
How is Suxamethonium metabolized?
It is broken down by pseudocholinesterase in plasma after diffusing away from the synaptic cleft.
p.24
Mechanisms of Action of Inhalational Anaesthetics
What central nervous system effects can Glycopyrrolate cause?
Headache and sedation, despite not crossing the BBB.
p.2
Physiochemical Properties of Volatile Agents
What is the molecular weight of isoflurane and enflurane?
Both have a molecular weight of 184.
p.26
Opioid Pharmacology and Effects
What should be done if an opioid-dependent patient is on a methadone program?
Ascertain their daily requirements and continue this dosage perioperatively.
p.19
Cardiovascular Effects of Inhalational Agents
What cardiovascular effects does Sugammadex have?
It is cardiovascularly stable and avoids the need for anticholinesterase and antimuscarinic agents.
p.16
Neuromuscular Blocking Drugs Classification and Mechanism
What are the respiratory side effects of neostigmine?
Bronchoconstriction and increased secretions.
p.8
Neuromuscular Blocking Drugs Classification and Mechanism
What is the mechanism of action of sugammadex?
It completely envelops aminosteroid neuromuscular blockers, preventing them from interacting with the nicotinic acetylcholine receptor.
p.11
Metabolism and Toxicity of Inhalational Anaesthetics
What are the two modes of metabolism for Atracurium?
Ester hydrolysis and Hofmann degradation.
p.11
Metabolism and Toxicity of Inhalational Anaesthetics
What is the effect of acidosis and cold on Hofmann degradation?
They slow the rate of degradation.
p.2
Physiochemical Properties of Volatile Agents
What is the significance of fluorine in inhalational agents?
Fluorine lowers molecular weight, increases blood solubility, and stabilizes ethers.
p.6
Neuromuscular Blocking Drugs Classification and Mechanism
What is the result of the persistent depolarization caused by suxamethonium?
Inactivation of Na+ channels, preventing repolarization and causing flaccid paralysis.
p.12
Metabolism and Toxicity of Inhalational Anaesthetics
How is Mivacurium metabolized?
By plasma cholinesterases.
p.22
Metabolism and Toxicity of Inhalational Anaesthetics
What are the central features of acute central anticholinergic syndrome?
Altered mental status, disorientation, hallucinations, agitation, ataxia, somnolence, and coma.
p.26
Neuromuscular Blocking Drugs Classification and Mechanism
What actions are associated with KOP receptors?
Spinal analgesia, sedation, and meiosis.
p.23
Cardiovascular Effects of Inhalational Agents
What cardiovascular effects does Atropine have?
Tachycardia and may precipitate arrhythmias.
p.9
Neuromuscular Blocking Drugs Classification and Mechanism
What are the uses of Pancuronium bromide?
To provide muscle relaxation for intubation, ventilation, and surgery.
p.12
Cardiovascular Effects of Inhalational Agents
What are the potential effects of high doses of Mivacurium?
Histamine release, which can precipitate hypotension and bronchospasm.
p.20
Anticholinesterase Agents and Their Uses
What is the clinical use of atropine?
Treatment of bradycardia.
p.21
Anticholinesterase Agents and Their Uses
How is glycopyrrolate primarily excreted?
Urine and bile (majority unchanged).
p.18
Cardiovascular Effects of Inhalational Agents
What are the central nervous system effects of Edrophonium?
Miosis, blurred vision, and muscle contraction at low doses.
p.22
Metabolism and Toxicity of Inhalational Anaesthetics
What skin-related side effects can occur?
Impaired sweating leading to hot, dry, and vasodilated skin, with possible pyrexia, especially in children or in cases of overdose.
p.19
Mechanisms of Action of Inhalational Anaesthetics
How does Sugammadex achieve rapid reversal of neuromuscular blockade?
By creating a concentration gradient between plasma and the neuromuscular junction, causing muscle relaxants to diffuse away from the NMJ into plasma.
p.25
Opioid Pharmacology and Effects
What is tolerance in the context of opioids?
Tolerance refers to a decreasing response to repeated dosing of a drug, requiring larger doses to achieve the same effect.
p.9
Metabolism and Toxicity of Inhalational Anaesthetics
How is Pancuronium bromide metabolized?
35% hepatic metabolism to 3- and 17-hydroxy and 3,17-dihydroxypancuronium.
p.25
Opioid Pharmacology and Effects
What are the two theories explaining the development of opioid tolerance?
Tolerance may develop due to receptor down-regulation or uncoupling of the receptor from its G-protein with repeated doses.
p.26
Neuromuscular Blocking Drugs Classification and Mechanism
Where are DOP receptors primarily located and what is their main action?
Located in the brain; they primarily provide analgesia and have antidepressant effects.
p.17
Factors Affecting Speed of Onset of Anaesthesia
What is the duration of action of Neostigmine?
Max effect in 7–11 minutes, lasting about 4 hours.
p.2
Metabolism and Toxicity of Inhalational Anaesthetics
What are the harmful effects of inhalational anaesthetic agents?
Hepato- and nephrotoxicity, bone marrow depression, and halothane hepatitis.
p.17
Cardiovascular Effects of Inhalational Agents
What are the gastrointestinal effects of Neostigmine?
Increased secretions, peristalsis, nausea, and vomiting.
p.22
Metabolism and Toxicity of Inhalational Anaesthetics
What eye-related side effects can occur due to these agents?
Mydriasis causing photophobia, loss of accommodation (cycloplegia), dry eyes (xerophthalmia), and risk of raised intra-ocular pressure in closed angle glaucoma.
p.10
Neuromuscular Blocking Drugs Classification and Mechanism
What is a common use of Suxamethonium?
Rapid sequence induction for fast onset of relaxation (45 seconds).
p.26
Opioid Pharmacology and Effects
How should post-operative pain control be managed in an opioid-dependent patient?
Continue their baseline opioid dosage and provide additional pain relief as needed, considering their tolerance.
p.3
Mechanisms of Action of Inhalational Anaesthetics
What is the multi-site hypothesis regarding inhalational agents?
Different agents alter higher CNS functions at different concentrations, implying multiple sites of action.
p.18
Metabolism and Toxicity of Inhalational Anaesthetics
What gastrointestinal effects can Edrophonium cause?
Increased secretions, peristalsis, nausea, and vomiting.
p.18
Anticholinesterase Agents and Their Uses
What distinguishes a myasthenic crisis from a cholinergic crisis when using Edrophonium?
In a myasthenic crisis, strength improves; in a cholinergic crisis, it worsens.
p.16
Anticholinesterase Agents and Their Uses
What are the uses of Physostigmine?
Topical eye drops in the treatment of glaucoma.
p.26
Neuromuscular Blocking Drugs Classification and Mechanism
What are the main actions of MOP receptors when stimulated?
Analgesia, physical dependence, respiratory depression, reduced peristalsis, euphoria, and meiosis.
p.14
Neuromuscular Blocking Drugs Classification and Mechanism
What is the duration of action for Rocuronium bromide?
Approximately 45 minutes.
p.4
Minimum Alveolar Concentration (MAC)
What is MAC 50?
The concentration at which 50% of the population fails to respond to a standard noxious stimulus.
p.12
Metabolism and Toxicity of Inhalational Anaesthetics
What can prolong the effect of Mivacurium?
Genetically low levels of plasma cholinesterases in the patient.
p.4
Factors Affecting Speed of Onset of Anaesthesia
What factors decrease MAC?
Increasing age, pregnancy, hypothermia, hyponatraemia, hypothyroidism, hypotension, hypoxia, metabolic acidosis, acute alcohol intake, narcotics, ketamine, benzodiazepines, α2 agonists, lithium.
p.3
Mechanisms of Action of Inhalational Anaesthetics
What is the role of excitatory neurotransmitters in the action of inhalational anesthetics?
They are thought to be inhibited.
p.18
Cardiovascular Effects of Inhalational Agents
What are the cardiovascular effects of Edrophonium?
Bradycardia, hypotension, and reported cardiac arrest.
p.10
Neuromuscular Blocking Drugs Classification and Mechanism
What can prolonged neuromuscular blockade with repeated dosing of Suxamethonium lead to?
Type 2 block, which shows characteristics of non-depolarizing agents and cannot be reversed with neostigmine.
p.7
Factors Affecting Speed of Onset of Anaesthesia
What factors affect the speed of recovery from non-depolarising muscle relaxation?
Initial dose, drug metabolism, and drug interactions.
p.16
Anticholinesterase Agents and Their Uses
What is the treatment for organophosphorus poisoning?
Antimuscarinic agents such as atropine and pralidoxime.
p.16
Anticholinesterase Agents and Their Uses
Why is neostigmine usually given with an antimuscarinic agent?
To offset unpleasant effects.
p.9
Cardiovascular Effects of Inhalational Agents
What are some effects of Pancuronium bromide?
Stimulates SNS, may block reuptake of noradrenaline, causes tachycardia, sweating, flushing, and salivation.
p.2
Physiochemical Properties of Volatile Agents
How does halogenation affect inhalational agents?
Halogenation reduces flammability and influences metabolic stability.
p.13
Neuromuscular Blocking Drugs Classification and Mechanism
What is a potential effect of prolonged use of Vecuronium Bromide?
Critical illness myopathy.
p.22
Metabolism and Toxicity of Inhalational Anaesthetics
What are some peripheral features of acute central anticholinergic syndrome?
Dry mouth, mydriasis, blurred vision, paralytic ileus, urinary retention, tachycardia, and hot, dry, vasodilated skin.
p.26
Neuromuscular Blocking Drugs Classification and Mechanism
What effects do NOP receptors have when stimulated?
Anxiety, depression, effects on learning and memory, involvement in tolerance, and may set the body’s pain threshold.
p.23
Mechanisms of Action of Inhalational Anaesthetics
What central nervous system effects can Atropine cause?
It can cause central anticholinergic syndrome and has antiemetic effects.
p.1
Factors Affecting Speed of Onset of Anaesthesia
How does cardiac output influence the onset of anesthesia?
High cardiac output leads to more effective uptake from the alveolus, resulting in a slower rise in P a and slower onset, while low cardiac output allows for quicker uptake and faster onset.
p.1
Factors Affecting Speed of Onset of Anaesthesia
What is the second gas effect?
The second gas effect refers to the influence that N2O has on the speed of onset of anesthesia of a second gas (volatile), leading to a faster rise in P a.
p.2
Physiochemical Properties of Volatile Agents
What is the molecular weight of desflurane?
Desflurane has a molecular weight of 168.
p.7
Mechanisms of Action of Inhalational Anaesthetics
How do non-depolarising neuromuscular blocking drugs exert their effects?
They bind to the α subunits of the nicotinic acetylcholine receptors (nAChR) and competitively inhibit acetylcholine (ACh).
p.7
Metabolism and Toxicity of Inhalational Anaesthetics
What is the effect of acidosis and hypothermia on atracurium?
They slow down Hoffman degradation, prolonging the effects of atracurium.
p.10
Neuromuscular Blocking Drugs Classification and Mechanism
What are the routes of administration for Suxamethonium?
IV (intravenous) and IM (intramuscular).
p.3
Mechanisms of Action of Inhalational Anaesthetics
What is the critical volume hypothesis?
It states that sufficient inhalational agents dissolve into neuronal lipid membranes, distorting ion channels and impairing synaptic transmission.
p.14
Mechanisms of Action of Inhalational Anaesthetics
How does Rocuronium bromide work at the neuromuscular junction?
It competitively inhibits ACh at nicotinic receptors.
p.6
Neuromuscular Blocking Drugs Classification and Mechanism
What biological properties should an ideal neuromuscular blocker have?
Analgesic, no systemic effects other than neuromuscular blockade, and no toxic effects.
p.14
Metabolism and Toxicity of Inhalational Anaesthetics
What is the metabolic pathway for Rocuronium bromide?
Only 5% is metabolized by the liver; excreted in bile (60%) and urine (40%).
p.14
Cardiovascular Effects of Inhalational Agents
What effect can high doses of Rocuronium bromide have?
Can exert a vagolytic effect, causing tachycardia.
p.20
Anticholinesterase Agents and Their Uses
What is glycopyrrolate used for?
To reduce excessive secretions during procedures.
p.19
Mechanisms of Action of Inhalational Anaesthetics
What is the mechanism of action of Sugammadex?
It encapsulates rocuronium and vecuronium in its lipophilic core, preventing them from interacting with acetylcholine receptors at the neuromuscular junction.
p.24
Metabolism and Toxicity of Inhalational Anaesthetics
What are some common antimuscarinic side effects of Glycopyrrolate?
Dry mouth, urinary retention, and blurred vision.
p.26
Opioid Pharmacology and Effects
What is the concern for abstinent patients regarding opioid use for pain relief?
They may be reluctant to use opioids, but appropriate use is not shown to precipitate a relapse.
p.19
Metabolism and Toxicity of Inhalational Anaesthetics
What is the excretion route for Sugammadex?
Both cyclodextrin and cyclodextrin-aminosteroid complex are excreted in urine.
p.7
Neuromuscular Blocking Drugs Classification and Mechanism
What is the effect of magnesium sulphate on neuromuscular blockers?
It prolongs the action of neuromuscular blockers by inhibiting the release of acetylcholine at the neuromuscular junction.
p.3
Mechanisms of Action of Inhalational Anaesthetics
What effect do volatile agents have on GABA receptors?
They lead to an accumulation of GABA, activating the GABA A receptor and causing hyperpolarization of the cell membrane.
p.10
Factors Affecting Speed of Onset of Anaesthesia
What is the absorption rate of Suxamethonium at the neuromuscular junction?
Only 20% of the dose reaches the NMJ due to rapid hydrolysis.
p.23
Metabolism and Toxicity of Inhalational Anaesthetics
What is the effect of Atropine on sweating?
It inhibits sweating, which may cause hyperpyrexia in children.
p.26
Opioid Pharmacology and Effects
Why should pethidine be avoided in opioid-dependent patients?
Large doses may cause accumulation of the proconvulsant metabolite nor-pethidine.
p.22
Metabolism and Toxicity of Inhalational Anaesthetics
What genitourinary side effects are associated with these agents?
Reduced urinary tract peristalsis and detrusor muscle tone, combined with increased sphincter tone causing urinary retention.
p.20
Anticholinesterase Agents and Their Uses
What is the use of benztropine?
As an anti-parkinsonian drug.
p.19
Physiochemical Properties of Volatile Agents
What is the absorption and distribution profile of Sugammadex?
It is biologically inactive, has no protein binding.
p.7
Metabolism and Toxicity of Inhalational Anaesthetics
How do drugs that induce liver enzymes affect aminosteroids?
They reduce the effects of aminosteroids, increasing the necessary dose.
p.16
Neuromuscular Blocking Drugs Classification and Mechanism
What gastrointestinal effects does neostigmine have?
Increased secretions, peristalsis, nausea, and vomiting.
