Extra Cards (from AI) Flashcards
(35 cards)
Who is credited with first using d-tubocurarine during ether anesthesia in 1942?
Griffith and Johnson
First documented use of d-tubocurarine in anesthesia.
What historical event related to NMBAs occurred in 1935?
H. King isolated curare from Chondodendron tomentosum
Isolation of curare marked significant progress in the understanding of neuromuscular blocking agents.
What is the primary mechanism of action for acetylcholine release at the presynaptic terminal?
Associated with the influx of calcium
NMBAs block both pre- and post-synaptic acetylcholine receptors.
List three substances or conditions that can potentiate muscle relaxants by inhibiting calcium influx.
- Magnesium (competitively inhibits calcium influx)
- Calcium channel blockers
- Aminoglycosides
These substances can enhance the effects of neuromuscular blocking agents.
What are the two types of postsynaptic acetylcholine receptors based on their lifespan?
- Mature (life span 2 weeks)
- Immature (24 hour life span and are more easily depolarized)
Understanding receptor types is crucial for predicting response to NMBAs.
Describe the key characteristics of a Non-competitive Block (Phase I) caused by a depolarizing NMBA like succinylcholine.
- Not metabolized by acetylcholinesterase
- Drugs detach and re-attach to receptors
- Cleared from the junction and hydrolyzed by plasma(pseudo)-cholinesterases
- Initial binding causes fasiculation followed by relaxation
- Perijunctional sodium channels are not activated after initial depolarization
Understanding the mechanism of depolarizing NMBAs is essential for clinical practice.
What characterizes a Phase II (non-depolarizing) Block, and how is it typically reversed?
Characterized by tetany or train of four fade. Reversed by acetylcholinesterase inhibitors
This phase can occur with high doses of depolarizing relaxants.
What is a Desensitization Block, and what can cause it?
Acetylcholine binds to the receptor but does not activate it. Caused by high concentrations of agonist, nicotine, inhalation anesthetics, barbiturates, alcohols, local anesthetics, phenothiazines, verapamil, and polymixin B
Desensitization blocks complicate the neuromuscular blocking process.
What is a Channel Block, and can it be reversed by acetylcholinesterase inhibitors?
A non-competitive prevention of the opening and closing of the acetylcholine receptor. Cannot be reversed by acetylcholinesterase inhibitors
Understanding channel blocks is vital for managing NMBAs.
Provide examples of drugs that cause a ‘closed channel block’ and an ‘open channel block.’
- Closed channel block: Antibiotics, cocaine, quinidine, tricyclic antidepressants, naltrexone, naloxone
- Open channel block: Pancuronium, gallamine, succinylcholine
Different blocks have distinct clinical implications.
What is the primary function of acetylcholinesterase within the neuromuscular junction?
Hydrolyzes acetylcholine to acetic acid and choline
This process is crucial for terminating the action of acetylcholine.
Beyond the neuromuscular junction, where else is acetylcholinesterase located?
In parasympathetic nerve endings
Inhibition leads to increased salivation and decreased heart rate.
What structural feature is characteristic of all NMBAs?
At least one quaternary amine group
Most NMBAs contain two amine groups.
Which type of NMBA has a higher potential for histamine release?
Benzylisoquinolines (e.g., d-tubocurarine, mivacurium, and atracurium)
Steroidal NMBAs generally have less histamine release potential.
What are the signs and symptoms of histamine release from NMBAs?
- Erythema
- Blistering
- Tachycardia
- Hypotension
Recognizing these symptoms is crucial for patient safety.
Name two strategies to prevent or decrease histamine release during NMBA administration.
- Slower, graduated, or repetitive administration
- Pre-medication with H1 or H2 blockers
These strategies can mitigate adverse reactions during anesthesia.
Define ‘Potency’ and ‘Onset’ as pharmacologic variables for NMBAs.
- Potency: Effective dose (ED95 and ED50)
- Onset: Interval between injection and maximal block
These variables are critical for dosing and timing in clinical settings.
Define ‘Clinical duration of action,’ ‘Recovery Index,’ and ‘Total duration of action’ for NMBAs.
- Clinical duration of action (DUR25 and DUR95): Interval between injection and recovery of twitch response
- Recovery Index: Speed of offset of action
- Total duration of action: Between injection and recovery of TOF ratio to >=0.7
Understanding these definitions helps in monitoring patient recovery.
How are NMBAs typically administered, and what is the predictability of different routes?
Administered intravenously (IV) for rapid onset. IM or SQ is less predictable
Oral administration is not effective for NMBAs.
How does age influence the pharmacokinetics of NMBAs in children and the elderly?
- Children: Higher doses needed, more sensitive neuromuscular junction
- Elderly: Delayed metabolism and excretion
Age-related changes impact drug effectiveness and safety.
How do pregnancy and temperature affect NMBA pharmacokinetics?
- Pregnancy: Increased potency and duration when magnesium is used
- Temperature (Hypothermia): Increased duration
These factors must be considered in anesthetic management.
Which two NMBAs are primarily metabolized by plasmacholinesterase?
- Succinylcholine
- Mivacurium
This metabolism is important for understanding their duration of action.
How do homozygous and heterozygous atypical plasma cholinesterase affect the duration of NMBA blockade?
- Heterozygous (1:480): Minimal effects
- Homozygous (1:3200): Prolonged blockade for hours
The Dibucaine test is used to identify enzyme function.
List several conditions or drugs that can cause acquired cholinesterase deficiency.
- Cholinesterase inhibitors (neostigmine and pyridostigmine)
- Pancuronium
- Metoclopramide
- Liver failure
- Burn injury
- Renal insufficiency
- Pregnancy
Recognizing these factors is essential for managing NMBAs.
