MBB: Pain & Anesthesia
Terms in this set (74)
What are the two general types of neuromuscular blockers?
Depolarizing and non-depolarizing.
What are three side effects that are present with a depolarizing neuromuscular blocker, but not with a non-depolarizing neuromuscular blocker?
Hyperkalemia, increased intraocular and intragastric pressure, and muscle pain.
Why do depolarizing neuromuscular blockers cause hyperkalemia?
Because when cells depolarize, sodium rushes in, and potassium rushes out to maintain electrical neutrality.
What is the mechanism of action of depolarizing neuromuscular blockers?
They are non-competitive antagonists which act on nicotinic cholinergic receptors and depolarizes the neuromuscular end plate.
What is the mechanism of action of non-depolarizing neuromuscular blockers?
They are competitive atagonists which prevent the action of acetylcholine at the skeletal muscle end plate.
What is the only depolarizing neuromuscular blocker used clinically?
What enzyme hydrolyzes succinylcholine in the plasma?
Describe the onset and duration of succinylcholine.
It has a rapid onset and is very short-acting.
What receptor is commonly mutated in patients who are prone to developing malignant hyperthermia?
The ryanodine receptor.
What agents can trigger malignant hyperthermia?
Succinylcholine and inhalational agents, except for nitrous oxide.
Why do some patients remain paralyzed for much longer than expected after being given succinylcholine?
Due to genetic variation in pseudocholinesterase.
What is the pathophysiology of malignant hyperthermia?
It causes uncontrolled muscle contraction with signs of hypermetabolism and muscle breakdown.
What is the treatment for malignant hyperthermia, and how does this agent work?
Dantrolene, which prevents the intracellular release of calcium from the sarcoplasmic reticulum of skeletal muscle.
What medications are commonly given to reverse non-depolarizing neuromuscular blockers, and how do these medications work?
Neostigmine or pyridostigmine, which are acetylcholinesterase inhibitors, so they increase acetylcholine concentrations at the neuromuscular junction and reverse the neuromuscular blockade.
When neostigmine or pyridostigmine are given to reverse non-depolarizing neuromuscular blockers, what medications are given in addition, and why?
Atropine or scopolomine, to prevent excessive muscarinic effects.
Which spasmolytic is also used as an antidote for malignant hyperthermia and neuroleptic malignant syndrome?
Which spasmolytic could also be used in the management of seizures caused by an overdose of local anesthetic?
What are the two broad categories of local anesthetics?
Esters and amides.
How are esters metabolized?
How are amides metabolized?
By liver enzymes.
How can the duration of action of a local anesthetic be increased?
By adding a vasoconstrictor such as cocaine or epinephrine.
How do local anesthetics work?
They block voltage-dependent sodium channels and influx of sodium, thus blocking the propagation of a nerve action potential.
What nerves are most easily blocked by local anesthetics?
Smaller, myelinated, rapidly-firing fibers.
What are the possible toxic CNS effects of local anesthetics?
They can lead to tonic-clonic seizures at high doses or after direct cerebral injection.
What are the possible toxic cardiovascular effects of local anesthetics?
They depress myocardial automaticity, contractility, and conduction velocity, and may lead to cardiac arrhythmia and circulatory collapse.
What disease can be caused by a by-product of prilocaine metabolism?
How can local anesthetics cause allergic reactions?
Ester metabolites, most commonly para-aminobenzoic acid, can cause allergic reactions.
How are the seizures caused by local anesthetic overdose treated?
They are usually self-terminating, but can be treated with benzodiazepines.
What medication is used to treat cardiovascular toxicity from local anesthetics?
How can succinylcholine affect the heart rate, and why?
It can cause bradycardia due to activation of cardiac muscarinic receptors.
How can pancuronium, a non-depolarizing neuromuscular blocker, affect the heart rate, and why?
It can cause tachycardia due to blockade of cardiac muscarinic receptors.
What is the hypothesized mechanism of action for inhaled anesthetics?
Enhancement of inhibitory postsynaptic ion channels (GABA) and inhibition of excitatory presynaptic ion channels.
What characteristics of an inhaled anesthetic will allow for the fastest induction?
Low solubility, high ventilation rate, low pulmonary blood flow, and high partial pressure.
What is the minimum alveolar anesthetic concentration (MAC)?
The alveolar concentration required to eliminate the response to a standard stimulus in 50% of patients.
What are the cardiovascular effects of inhaled anesthetics?
Most decrease vascular resistance, leading to a decrease in blood pressure. Halothane and enflurane are myocardial depressants and depress cardiac output. Nitrous oxide has little cardiac effect.
What are the respiratory effects of inhaled anesthetics?
They all decrease tidal volume and minute ventilation.
Which intravenous anesthetic would be the optimal choice for patients with limited cardiac reserve, and why?
Etomidate, because it causes minimal change in cardiac function and blood pressure.
Which intravenous anesthetic increases both heart rate and systemic blood pressure?
Which two intravenous anesthetics decrease systemic blood pressure?
Propofol and barbiturates.
Which intravenous anesthetic has anti-emetic properties and can be used for sedation as well as anesthesia?
Which type of intravenous anesthetic decreases cerebral blood flow?
Which type of intravenous anesthetic can be used for sedation, has amnestic properties, and preserves ventilation at low doses?
Which intravenous anesthetic is a dissociative anesthetic, increases intracranial pressure, and can cause hallucinations?
Which intravenous anesthetic can cause adrenal suppression?
What are the four stages of anesthesia?
Analgesia, disinhibition, surgical anesthesia, and medullary depression.
At what stage of anesthesia are pulse and blood pressure increased?
Disinhibition; the second stage.
Which intravenous benzodiazepine is the optimal choice for conscious sedation, and why?
Midazolam, because it has a short duration of action, is non-irritating on injection, and has a high therapeutic index.
Which two intravenous anesthetics would be acceptable options for a hemodynamically unstable trauma patient, and why?
Etomidate would be the best choice, because it has the fewest hemodynamic side effects. Ketamine would also be an acceptable choice, but it can act as a myocardial depressant at high doses, so there would be more risk with ketamine than with etomidate.
What is general anesthesia?
An altered physiologic state characterized by loss of consciousness, analgesia of the entire body, amnesia, and, to some degree, muscle relaxation.
When is a basic drug ionized?
When the pH is less than the pKA.
What is the most common life-threatening effect of a local anesthetic overdose?
Local anesthetics preferentially bind to which type of channels?
Open and activated channels.
What is nociception?
The neural process of encoding and processing noxious stimuli.
What is neuropathic pain?
Pain initiated or caused by a primary lesion or dysfunction in the peripheral nervous system.
What is central pain?
Pain initiated or caused by a primary lesion or dysfunction in the central nervous system.
What are the most common co-occurring mood disorders with chronic pain?
Anxiety, depression, and PTSD.
How do opiates interact with G-proteins?
They couple with inhibitory G-proteins, inhibiting neuronal depolarization, and decrease cAMP via G-protein coupling.
How do opiates affect polymodal nociceptors?
They decrease depolarization of polymodal nociceptors.
How do opiates affect the inflammatory response?
They decrease the release of pro-inflammatory neuropeptides.
How do opiates/mu-agonists affect potassium channels in the spine?
They open potassium channels that increase membrane hyperpolarization, thereby evoking an inhibitory post-synaptic potential.
Name five substances that are inhibited by opiates.
Acetylcholine, norepinephrine, serotonin, glutamate, and substance P.
What is the evidence for long-term effectiveness of opiates?
Four meta-analyses showed no reduction in pain with long-term use of opiates.
How do NSAIDs/selective COX-2 inhibitors relieve pain?
Inhibition of COX-2 prevents production of PGE2, which sensitizes nociceptors.
What is nociceptive pain?
Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors.
Why is hypertension a common side effect of NSAID use?
Because NSAIDs interfere with renal sodium clearance and reduce the effects of hypertensive drugs.
What two general categories of drugs are effective for management of neuropathic pain?
Antidepressants and anticonvulsants.
Which type of antidepressant is most effective for management of neuropathic pain?
Which two types of anticonvulsant drugs are effective for management of neuropathic pain?
Calcium channel modulators and sodium channel blockers.
Name three calcium channel modulators used for neuropathic pain.
Gabapentin, preglabin, and levetiracetam.
Name two sodium channel blockers used for neuropathic pain.
Carbamazepine and lamotrigine.
What is the mechanism by which tricyclic antidepressants relieve neuropathic pain?
Monoamines potentiate the descending inhibitory pathway.
What is trigeminal neuralgia?
Episodes of intense, stabbing pain in the distribution of the second division of the trigeminal nerve.
What is the first-line drug treatment for trigeminal neuralgia?
What is the most common dangerous side effect of Carbamazepine, which must be watched for by monitoring blood counts?