MasterPass 2 PHARMA 3

10–25%.

Aminosteroid non-depolarising muscle relaxant.

2 mg/mL in 5 and 10 mL vials.

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.

0.2 mg/mL.

It binds to the α-subunit but does not stimulate it to open the ion channel.

Morphine seems to cause uncoupling of its receptors but not down-regulation.

Reversal of neuromuscular blockade caused by non-depolarising muscle relaxants.

0.1 mg/kg.

Competitive inhibition of ACh at nicotinic receptors at the neuromuscular junction.

They are tertiary amines.

A benzylisoquinolinium non-depolarising muscle relaxant.

Approximately 45 minutes.

0.5 mg/kg.

Na+, K+, and Ca2+ ions.

Short acting, medium acting, and long acting.

In 1.5 minutes when given 3 minutes after an intubating dose.

10–20 minutes.

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).

An antimuscarinic drug.

48.5 °C.

Halothane (0.75).

2 mg/mL in 2 mL vials.

Halogenated hydrocarbon.

1.4

Myasthenia gravis.

It acts as a competitive antagonist at muscarinic receptors ('vagolytic').

Most are halogenated ethers, except halothane and nitrous oxide.

Bradycardia and hypotension.

5%.

It increases the delivery of the drug to the alveolus and leads to a more rapid rise in alveolar partial pressure (P a).

To decrease oral secretions, attenuate effects of anticholinesterases, treat bradycardia, and manage hyperhidrosis.

10%.

They inhibit the action of acetylcholinesterase by occupying its active site, preventing it from breaking down acetylcholine.

0.2 mg/kg.

Aminosteroid non-depolarising muscle relaxant.

Binds to the esteratic site of acetylcholinesterase (AChE), increasing the availability of acetylcholine (ACh) at the neuromuscular junction.

The receptor undergoes a conformational change, opening the central pore for ion flow.

0.1 mg/kg.

Anticholinesterases, such as neostigmine.

100 minutes.

Around 15–20 minutes.

Duration of anaesthesia, gender, alkalosis, hypertension, anaemia, magnesium and potassium levels.

A synthetic quaternary amine.

By increasing the concentration of acetylcholine at the neuromuscular junction.

Metabolised by plasma esterases with some hepatic metabolism; excreted in bile and urine.

Sevoflurane decreases heart rate (↓).

1−2%.

Desflurane has no significant effect on cardiac output (↔).

70%.

Their antagonistic action on the 'rest and digest' activity of glands, smooth muscle, and cardiac muscle.

It carbamylates the active site of acetylcholinesterase, prolonging the effects of acetylcholine.

It is composed of five subunits: two α, one β, one δ, and one γ, arranged around a central pore.

To reverse the effects of non-depolarising neuromuscular blocking drugs by increasing the amount of acetylcholine available.

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).

Aminosteroid non-depolarising muscle relaxant.

It is a synthetic quaternary amine.

Sevoflurane has a faster onset of anesthesia.

Hyoscine and atropine can cross the BBB; glycopyrrolate cannot.

Because they are bulky and polar, making it difficult for them to cross cell membranes.

Minimal metabolism; excreted unchanged in urine.

Miosis, blurred vision, and muscle contraction at low doses; potential neuromuscular transmission blockage at high doses.

2–3 hours.

Halothane.

Reversal of competitive neuromuscular blocking drugs and treatment of constipation in the ICU.

It oxidizes the cobalt atom in vitamin B12, leading to bone marrow depression.

Dry mouth, urinary retention, and blurred vision.

The concentration effect occurs when N2O is used in high concentration, leading to a disproportionate rise in alveolar partial pressures of other gases.

It strongly inhibits the NMDA receptor.

Antisialagogue (reduces saliva production).

A bronchodilator.

To treat motion sickness, post-operative nausea, and opioid-induced nausea.

They are used to facilitate upper gastrointestinal endoscopy.

ED50 is the dose required for 50% depression in twitch height, and ED95 is for 95% depression.

Yes, but it is not licensed for its reversal.

A benzylisoquinolinium non-depolarising muscle relaxant.

0.05 mg/kg.

<0.01%

Sevoflurane has a lower blood:gas coefficient of 0.6, making it less soluble in blood than isoflurane.

Competitive inhibition of ACh at nicotinic receptors at the neuromuscular junction.

pH 3.5–5.

Halothane.

Lipid solubility (oil:gas coefficient) and potency (MAC).

Inspired concentration, alveolar minute ventilation, functional residual capacity, cardiac output, and the concentration and second gas effect.

To decrease secretions, treat bradycardia, and organophosphate poisoning.

0.27 L/kg.

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.

Isoflurane decreases myocardial work and oxygen consumption.

Hyoscine hydrobromide crosses the blood-brain barrier, while hyoscine butylbromide does not.

1.3 MAC is required to prevent coughing and movement during endotracheal intubation.

It can manifest as reversible transaminitis or fulminant hepatitis, with risk factors including repeated exposure, female sex, obesity, and middle age.

Arrhythmias, anaphylaxis, malignant hyperpyrexia, hyperkalaemia, myalgia, increased intraocular pressure, and prolonged neuromuscular blockade.

They are classified into two groups: Aminosteroids (e.g., vecuronium, rocuronium, pancuronium) and Benzylisoquinolinium esters (e.g., atracurium, mivacurium).

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.

Can cause sludge syndrome and death by paralysis of the respiratory muscles.

0.2–0.6 mg IV or IM.

Competitive inhibition of ACh at nicotinic receptors at the neuromuscular junction.

Trifluoroacetic acid, chloride and bromide ions.

50 mg/mL.

Halothane (20%).

1.15

An oxygen atom that destabilizes bonds between constituent atoms, leading to Hoffman degradation.

10%.

Binds to α-subunit of nicotinic receptors at the neuromuscular junction, causing chaotic depolarization and fasciculation before flaccid paralysis.

Atropine at 50%.

All decrease CMRO2.

0.15 L/kg.

Compound A can be produced from sevoflurane reacting with CO2 absorbents, but concentrations are usually below toxic thresholds.

Anxiety, adrenergic hyperactivity, malaise, abdominal cramps, sweating, and yawning.

Young age (infants and children) increases MAC.

Decreased bowel movement, paralytic ileus, and reduced lower esophageal sphincter pressure, risking exacerbation of reflux.

It is 7 times less potent than Vecuronium.

2 mg/kg for moderate block and 4 mg/kg for deep block.

As a mydriatic agent.

Phosphorylation of the active site of the enzyme.

Bradycardia and hypotension.

Isoflurane causes a significant decrease (↓↓) in SVR.

Succinylcholine or scoline.

It binds to the α subunit of the nAChR, causing depolarization and muscle fasciculations.

10 mg/mL.

It is not broken down by acetylcholine esterase, leading to sustained depolarization.

0.6 mg/kg allows intubation in 90–120 seconds.

Minimum Alveolar Concentration.

10%.

Reversal of neuromuscular blockade caused by non-depolarising muscle relaxants.

It can cause histamine release, leading to hypotension and bronchospasm.

Binds reversibly to the esteratic site of acetylcholinesterase, reducing the breakdown of acetylcholine.

Because it is not reliant on these organs for metabolism.

2 mg followed by 8 mg if no improvement in strength.

Dependence is the physical need for a drug to avoid withdrawal symptoms, while addiction involves compulsive drug-seeking behavior despite harm.

Increased anatomical dead space.

Reversal of neuromuscular blockade caused by rocuronium and vecuronium.

IM and IV.

MAC is additive when inhalational agents are administered simultaneously.

The bond releases halogen ions, which can be nephrotoxic.

At least 70% of all receptors must be occupied.

Rocuronium is less potent than vecuronium, requiring a higher dose to achieve the same degree of muscle relaxation.

It can lead to accumulation of the drugs and prolong their effects.

Miosis, blurred vision, muscle contraction at low doses, and neuromuscular transmission issues at high doses.

Competitive inhibition of ACh at nicotinic receptors at the neuromuscular junction.

0.2–0.4 mg IV or IM.

Hepatic metabolism by deacetylation.

It is a competitive antagonist at muscarinic receptors ('vagolytic').

10–40%.

Through hepatic metabolism.

15%.

Competitive antagonists of acetylcholine at muscarinic acetylcholine receptors.

Cheap, long shelf life, water-soluble, painless on injection, ultra-rapid onset, predictable duration, and no accumulation.

They reduce the activity of the parasympathetic nervous system.

Gamma amino butyric acid (GABA).

It is broken down by pseudocholinesterase in plasma after diffusing away from the synaptic cleft.

Halothane (20%).

Hyoscine (+++).

Headache and sedation, despite not crossing the BBB.

Both have a molecular weight of 184.

Ascertain their daily requirements and continue this dosage perioperatively.

1.8 hours.

It is cardiovascularly stable and avoids the need for anticholinesterase and antimuscarinic agents.

Bronchoconstriction and increased secretions.

It completely envelops aminosteroid neuromuscular blockers, preventing them from interacting with the nicotinic acetylcholine receptor.

Ester hydrolysis and Hofmann degradation.

They slow the rate of degradation.

Fluorine lowers molecular weight, increases blood solubility, and stabilizes ethers.

Inactivation of Na+ channels, preventing repolarization and causing flaccid paralysis.

By plasma cholinesterases.

Altered mental status, disorientation, hallucinations, agitation, ataxia, somnolence, and coma.

Spinal analgesia, sedation, and meiosis.

Tachycardia and may precipitate arrhythmias.

To provide muscle relaxation for intubation, ventilation, and surgery.

Tachycardia.

Histamine release, which can precipitate hypotension and bronchospasm.

Bronchodilation.

Treatment of bradycardia.

Bridion.

Urine and bile (majority unchanged).

Miosis, blurred vision, and muscle contraction at low doses.

Impaired sweating leading to hot, dry, and vasodilated skin, with possible pyrexia, especially in children or in cases of overdose.

By creating a concentration gradient between plasma and the neuromuscular junction, causing muscle relaxants to diffuse away from the NMJ into plasma.

Sarin and VX.

Tolerance refers to a decreasing response to repeated dosing of a drug, requiring larger doses to achieve the same effect.

35% hepatic metabolism to 3- and 17-hydroxy and 3,17-dihydroxypancuronium.

Tolerance may develop due to receptor down-regulation or uncoupling of the receptor from its G-protein with repeated doses.

4°C.

Located in the brain; they primarily provide analgesia and have antidepressant effects.

Increases HR.

Max effect in 7–11 minutes, lasting about 4 hours.

Hepato- and nephrotoxicity, bone marrow depression, and halothane hepatitis.

Increased secretions, peristalsis, nausea, and vomiting.

Mydriasis causing photophobia, loss of accommodation (cycloplegia), dry eyes (xerophthalmia), and risk of raised intra-ocular pressure in closed angle glaucoma.

0.9−1.3 L/kg.

Rapid sequence induction for fast onset of relaxation (45 seconds).

Continue their baseline opioid dosage and provide additional pain relief as needed, considering their tolerance.

Different agents alter higher CNS functions at different concentrations, implying multiple sites of action.

Increased secretions, peristalsis, nausea, and vomiting.

In a myasthenic crisis, strength improves; in a cholinergic crisis, it worsens.

Topical eye drops in the treatment of glaucoma.

Treatment of glaucoma.

Analgesia, physical dependence, respiratory depression, reduced peristalsis, euphoria, and meiosis.

3–10 μg/kg.

Approximately 45 minutes.

The concentration at which 50% of the population fails to respond to a standard noxious stimulus.

Genetically low levels of plasma cholinesterases in the patient.

Increasing age, pregnancy, hypothermia, hyponatraemia, hypothyroidism, hypotension, hypoxia, metabolic acidosis, acute alcohol intake, narcotics, ketamine, benzodiazepines, α2 agonists, lithium.

Hyoscine.

Tensilon.

They are thought to be inhibited.

Tachycardia.

Bradycardia, hypotension, and reported cardiac arrest.

Type 2 block, which shows characteristics of non-depolarizing agents and cannot be reversed with neostigmine.

Initial dose, drug metabolism, and drug interactions.

Antimuscarinic agents such as atropine and pralidoxime.

To offset unpleasant effects.

Stimulates SNS, may block reuptake of noradrenaline, causes tachycardia, sweating, flushing, and salivation.

Halogenation reduces flammability and influences metabolic stability.

Critical illness myopathy.

Dry mouth, mydriasis, blurred vision, paralytic ileus, urinary retention, tachycardia, and hot, dry, vasodilated skin.

Anxiety, depression, effects on learning and memory, involvement in tolerance, and may set the body’s pain threshold.

It can cause central anticholinergic syndrome and has antiemetic effects.

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.

10%.

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.

Desflurane has a molecular weight of 168.

They bind to the α subunits of the nicotinic acetylcholine receptors (nAChR) and competitively inhibit acetylcholine (ACh).

0.5–5 hours.

They slow down Hoffman degradation, prolonging the effects of atracurium.

Sweating.

IV (intravenous) and IM (intramuscular).

It states that sufficient inhalational agents dissolve into neuronal lipid membranes, distorting ion channels and impairing synaptic transmission.

It competitively inhibits ACh at nicotinic receptors.

Analgesic, no systemic effects other than neuromuscular blockade, and no toxic effects.

Only 5% is metabolized by the liver; excreted in bile (60%) and urine (40%).

1 hour.

Can exert a vagolytic effect, causing tachycardia.

10 minutes.

To reduce excessive secretions during procedures.

It encapsulates rocuronium and vecuronium in its lipophilic core, preventing them from interacting with acetylcholine receptors at the neuromuscular junction.

Dry mouth, urinary retention, and blurred vision.

They may be reluctant to use opioids, but appropriate use is not shown to precipitate a relapse.

As for neostigmine.

Atropine.

Both cyclodextrin and cyclodextrin-aminosteroid complex are excreted in urine.

It prolongs the action of neuromuscular blockers by inhibiting the release of acetylcholine at the neuromuscular junction.

They lead to an accumulation of GABA, activating the GABA A receptor and causing hyperpolarization of the cell membrane.

Only 20% of the dose reaches the NMJ due to rapid hydrolysis.

It inhibits sweating, which may cause hyperpyrexia in children.

0.2 L/kg.

Large doses may cause accumulation of the proconvulsant metabolite nor-pethidine.

Reduced urinary tract peristalsis and detrusor muscle tone, combined with increased sphincter tone causing urinary retention.

As an anti-parkinsonian drug.

It is biologically inactive, has no protein binding.

Weeks.

They reduce the effects of aminosteroids, increasing the necessary dose.

Increased secretions, peristalsis, nausea, and vomiting.