RNFA MASTER 2023/2024 QUESTION AND CORRECT ANSWER

RNFA MASTER 2023/2024 QUESTION AND CORRECT ANSWER Neuromuscular blockers - CORRECT ANSWER-Tubocurarine Atracurium Cisatracurium Mivacurium Rocuronium Pancuronium Vecuronium Succinylcholine AchE inhibitors - CORRECT ANSWER-Neostigmine Edrophonium Muscarinic Antagonists - CORRECT ANSWER-Glycopyrrolate Spasmolytics - CORRECT ANSWER-Dantrolene Diazepam Baclofen Tizanidine Gabapentin Progabide Glycine Idrocilamide Riluzole Dantrolene Botulinum toxin Cyclobenzaprine Neuromuscular blockers. - CORRECT ANSWER-Used during surgical procedures and in intensive care units to cause paralysis. NONDEPOLARIZING BLOCKERS - CORRECT ANSWER-• They are competitive antagonists. In small clinical doses they act predominantly at the nicotinic receptor site by competing with acetylcholine. Their action can be overcome by increasing the concentration of acetylcholine in the synaptic cleft; this can be achieved, for example, by administration of acetylcholinesterase inhibitors such as neostigmine or edrophonium. Anaesthesiologists use this strategy to shorten the duration of the neuromuscular blockade. • In larger doses, nondepolarizing blockers also enter the pore of the ion channel to cause a more intense motor blockade. This further weakens neuromuscular transmission and diminishes the ability of acetylcholinesterase inhibitors to antagonize the action of nondepolarizing blockers. • Nondepolarizing blockers may also block prejunctional sodium channels. As a result, they reduce the release of acetylcholine at the nerve ending. • During anesthesia, the IV administration of a nondepolarizing blocker first causes motor weakness; ultimately, skeletal muscles become totally flaccid and inexcitable to stimulation. Larger muscles (e.g. those of the trunk) are more resistant to block and recover more rapidly than smaller ones (e.g. muscles of the hand). DEPOLARIZING BLOCKERS - CORRECT ANSWER-Succinylcholine is the only depolarizing neuromuscular blocker used clinically in the USA. succinylcholine remains popular because it is the only ultrarapid onset/ultrashort duration neuromuscular blocker available. • Succinylcholine binds to the nicotinic receptor and acts like acetylcholine to cause depolarization of the end plate. This in turn spreads and depolarizes adjacent membranes, causing transient fasciculations, especially in chest and abdomen, though general anesthesia and prior administration of a small dose of a nondepolarizing muscle relaxant tends to attenuate them. Succinylcholine is not metabolized effectively at the synapse, therefore the membrane remains depolarized and unresponsive to additional impulses. A flaccid paralysis results. This is called Phase I block, or depolarization block. Phase I block is augmented, not reversed, by acetylcholinesterase inhibitors. • The onset of neuromuscular blockade is very rapid, usually within 1 minute. Because of its rapid hydrolysis by plasma butyrylcholinesterase (pseudocholinesterase), duration of neuromuscular block is 5-10 minutes. • With a single large dose, repeated doses, or prolonged continued infusion of succinylcholine (30-60 minutes) the membrane repolarizes; despite this repolarization, the membrane can't be depolarized again because it is desensitized. The channels behave as if they are in a prolonged closed state. This is called phase II block or desensitization block. Phase II block may be reversed by acetylcholinesterase inhibitors. PHARMACOKINETICS OF NEUROMUSCULAR BLOCKERS - CORRECT ANSWER-• All neuromuscular blocking agents contain one or two quaternary ammonium groups, which makes them highly polar and very poorly soluble in lipid. • Neuromuscular blockers are inactive if given by mouth. They are always given IV or IM. They penetrate membranes very poorly and do not enter cells or cross the bloodbrain barrier. NON-DEPOLARIZING BLOCKERS - CORRECT ANSWER-Highly ionized. They don't cross membranes well and have limited volume of distribution of 80-140 mL/Kg -not much larger than blood volume. They have durations of action that range from 20 to 90 minutes, which can be extended by supplemental dosing. Non-depolarizing blockers can be classified into: long-, intermediate-, and short-acting. SHORT-ACTING Mivacurium INTERMEDIATE-ACTING Atracurium Rocuronium Cisatracurium Vecuronium LONG-ACTING Tubocurarine Pancuronium METABOLISM - CORRECT ANSWER-The duration of neuromuscular blockade produced by nondepolarizing relaxants is strongly correlated with the elimination halflife. Drugs that are excreted by the kidney typically have longer half-lives, leading to longer durations of action. Drugs eliminated by the liver tend to have shorter half-lives and durations of action. Atracurium is inactivated by hydrolysis by non-specific plasma esterases and by a spontaneous reaction (Hoffman elimination). Duration of neuromuscular block produced by atracurium is not altered by the absence of renal function. One of atracurium metabolites is laudanosine. Laudanosine may cause transient hypotension and, in higher doses, seizures. Cisatracurium, a stereoisomer of atracurium, undergoes Hoffman elimination to form laudanosine. Because cisatracurium is more potent than atracurium and lower doses are required, laudanosine concentrations following cisatracurium administration are lower. Cisatracurium also causes less histamine release. Therefore, cisatracurium has largely replaced atracurium in clinical practice. Mivacurium has short duration of action. Hydrolysis by butyrylcholinesterase is the primary mechanism for inactivation of mivacurium. Not dependent on liver or kidney. Rocuronium has the most rapid onset among nondepolarizing blockers. Can be used as alternative to succinylcholine for rapid sequence intubation. DEPOLARIZING BLOCKERS - CORRECT ANSWER-The extremely short duration of action of succinylcholine (5-10 minutes) is due to its rapid hydrolysis by plasma (and hepatic) butyrylcholinesterase. Neuromuscular blockade by succinylcholine (and mivacurium) may be prolonged in patients with an abnormal variant of butyrylcholinesterase. Prolonged paralysis from succinylcholine caused by abnormal butyrylcholinesterase should be treated with continued mechanical ventilation until muscle function returns to normal. Because of the rarity of these variants, butyrylcholinesterase testing is not routine clinical procedure. ADVERSE EFFECTS - CORRECT ANSWER-... NON-DEPOLARIZING BLOCKERS - CORRECT ANSWER-• Some benzylisoquinolines may produce hypotension due to histamine release and ganglionic blockade. • Some ammonio steroids may produce tachycardia due to blockade of muscarinic receptors, which may lead to arrhythmias. These drugs should be used cautiously in patients with cardiovascular disease. HISTAMINE RELEASE - CORRECT ANSWER-Tubocurarine, and to a lesser extent, mivacurium and atracurium can produce hypotension as a result of histamine release. Tubocurarine is seldom used clinically at this time. Clinical signs of histamine release are erythema at the face and upper chest, a transient decrease in blood pressure, and an increase in heart rate. More severe reactions of histamine release include bronchospasm and circulatory collapse. Antihistamines can counteract responses that follow histamine release, particularly if given before the neuromuscular blocker. GANGLION BLOCKADE - CORRECT ANSWER-Tubocurarine may cause some blockade of nicotinic receptors of the autonomic ganglia and the adrenal medulla; this results in a fall in blood pressure and tachycardia. BLOCKADE OF CARDIAC MUSCARINIC RECEPTORS - CORRECT ANSWER-The ammoniosteroid pancuronium causes moderate tachycardia due to blockade of cardiac muscarinic receptors. The cardiovascular effects of pancuronium are usually not considered to be a clinically relevant problem (see table below). DEPOLARIZING BLOCKERS - CORRECT ANSWER-Succinylcholine stimulates all autonomic cholinoceptors: nicotinic receptors in both sympathetic and parasympathetic ganglia and muscarinic receptors in the heart. HISTAMINE RELEASE Succinylcholine has a slight tendency to release histamine. BRADYCARDIA - CORRECT ANSWER-Bradycardia may occur due to activation of muscarinic receptors. It can be prevented by thiopental, atropine, ganglionic blockers and non-depolarizing muscle relaxants. MUSCLE PAIN - CORRECT ANSWER-Important postoperative complaint. Due to damage produced by the unsynchronized contractions of adjacent muscle fibers. HYPERKALEMIA - CORRECT ANSWER-Due to loss of tissue potassium during depolarization. Risk of hyperkalemia is enhanced in patients with burns or muscle trauma. Hyperkalemia may lead to cardiac arrest or circulatory collapse. INCREASED INTRAOCULAR PRESSURE - CORRECT ANSWER-Due to extraocular muscle contractions. Despite this effect, the use of succinylcholine for eye operations is not contraindicated unless the anterior chamber is to be opened. INCREASED INTRAGASTRIC PRESSURE - CORRECT ANSWER-In some patients, the fasciculations caused by succinylcholine cause an increase in intragastric pressure. This makes emesis more likely, with the potential hazard of aspiration of gastric contents. MALIGNANT HYPERTHERMIA - CORRECT ANSWER-Malignant hyperthermia susceptibility, an autosomal dominant disorder of skeletal muscle, is one of the main causes of death due to anesthesia. The halogenated hydrocarbon anesthetics and succinylcholine alone have been reported to precipitate the response; however, most of the incidents arise from the combination of succinylcholine and an halogenated anesthetic. Treatment of malignant hyperthermia entails IV administration of dantrolene; dantrolene prevents Ca2+ and calmodulin from activating the RyR-1, thus blocking release of Ca2+ from the SR. CNS EFFECTS - CORRECT ANSWER-All neuromuscular blockers are virtually devoid of central effects following IV administration of ordinary clinical doses because of their inability to penetrate the blood- brain barrier. DRUG INTERACTIONS - CORRECT ANSWER-... ANESTHETICS - CORRECT ANSWER-Inhaled anesthetics (e.g. halothane, isoflurane and enflurane) increase neuromuscular blockade evoked by nondepolarizing muscle relaxants. ANTIBIOTICS - CORRECT ANSWER-Aminoglycosides produce neuromuscular blockade by inhibiting acetylcholine release from the preganglionic terminal (through competition with Ca2+) and to a lesser extent by stabilizing the postjunctional membrane. Tetracyclines can also produce neuromuscular blockade, possibly by chelation of Ca2+. EFFECTS OF DISEASE AND AGEING ON DRUG RESPONSE - CORRECT ANSWER-Several diseases can decrease or increase the neuromuscular blockade caused by nondepolarizing muscle relaxants. • Myasthenia gravis increases neuromuscular blockade caused by these agents. • Advanced age is often associated with a prolonged duration of action from nondepolarizing relaxants, probably due to decreased clearance of drugs by liver or kidneys. • Patients with severe burns and those with upper motor neuron disease are resistant to nondepolarizing muscle relaxants. This is probably because of proliferation of extrajunctional receptors, which requires additional nondepolarizing relaxant to block a sufficient number of receptors to produce neuromuscular blockade. DEPOLARIZING BLOCKERS: CONTRAINDICATIONS - CORRECT ANSWER-• Succinylcholine is contraindicated in persons with personal or familial history of malignant hyperthermia, skeletal muscle myopathies, and known hypersensitivity to the drug. • Succinylcholine is contraindicated in patients with major burns, multiple trauma, extensive denervation of skeletal muscle, or upper motor neuron injury, because succinylcholine may lead to severe hyperkalemia which may result in cardiac arrest. REVERSAL OF NONDEPOLARIZING NEUROMUSCULAR BLOCKADE - CORRECT ANSWER-• The acetylcholinesterase inhibitors neostigmine, pyridostigmine and edrophonium preserve endogenous acetylcholine and also act directly on the neuromuscular junction, therefore they can be used in the treatment of overdosage with competitive blocking agents. • Similarly, upon completion of a surgical procedure many anaesthesiologists employ neostigmine or edrophonium to reverse and decrease the duration of competitive neuromuscular blockade. A muscarinic antagonist (atropine or glycopyrrolate) is used concomitantly to prevent stimulation of muscarinic receptors and thereby avoid bradycardia. USES OF NEUROMUSCULAR BLOCKERS - CORRECT ANSWER-SURGICAL RELAXATION The main clinical use of the neuromuscular blockers is as adjuvants in surgical anesthesia to obtain relaxation of skeletal muscle. Neuromuscular blockers of short duration are often used to facilitate intubation with an endotracheal tube. CONTROL OF VENTILATION In patients who have ventilatory failure from various causes, e.g. obstructive airway disease, it is often desirable to control ventilation to provide adequate volumes and expansion of lungs. Paralysis is sometimes induced by administration of neuromuscular blockers to eliminate chest wall resistance and ineffective spontaneous ventilation. TREATMENT OF CONVULSIONS Neuromuscular blockers are sometimes used to attenuate or eliminate the peripheral manifestations of convulsions from such causes as epilepsy or local anesthetic toxicity. PREVENTION OF TRAUMA DURING ELECTROSHOCK THERAPY ECT therapy of psychiatric disorders occasionally is complicated by trauma to the patient; the seizures induced may cause dislocations or fractures. Neuromuscular blockers and thiopental are used. Succinylcholine or mivacurium are the neuromuscular blockers most often used because of the brevity of the relaxation SPASMOLYTIC DRUGS - CORRECT ANSWER-Spasticity is characterized by increase in tonic stretch reflexes and flexor muscle spasms together with muscle weakness. It is often associated with cerebral palsy, multiple sclerosis, and stroke. Drug therapy may ameliorate some of the symptoms of spasticity by modifying the stretch reflex arc or by interfering directly with skeletal muscle excitation-contraction coupling. DRUGS FOR CHRONIC SPASM - CORRECT ANSWER-... A. DRUGS THAT ACT IN THE CNS - CORRECT ANSWER-... DIAZEPAM - CORRECT ANSWER-Benzodiazepines facilitate the action of GABA at GABAA receptors. Diazepam has useful antispastic activity. It can be used in patients with muscle spasm of almost any origin, including local muscle trauma. It produces sedation in most patients at the doses required to reduce muscle tone. BACLOFEN - CORRECT ANSWER-Baclofen (p-chlorophenyl-GABA) is an orally active GABA agonist at GABAB receptors. Activation of GABAB receptors in the brain by baclofen results in hyperpolarization, probably by increased K+ conductance. Baclofen is useful for the alleviation of signs and symptoms of spasticity resulting from multiple sclerosis. Baclofen may also be of some value in patients with spinal cord injuries and other spinal cord diseases. TIZANIDINE - CORRECT ANSWER-Congener of clonidine. Agonist at α2-adrenergic receptors in the CNS. Reduces muscle spasticity. Short-acting. Assumed to act by increasing presynaptic inhibition of motor neurons. It also inhibits nociceptive transmission in the spinal dorsal horn. Used in spasticity associated with multiple sclerosis and spinal cord injury GABAPENTIN - CORRECT ANSWER-Gabapentin is an antiepileptic drug that has shown promise as spasmolytic and in patients with MS. Increases GABA release PROGABIDE - CORRECT ANSWER-GABAA and GABAB agonist. Reduces spasticity. GLYCINE - CORRECT ANSWER-Reduces spasticity. Inhibitory amino acid neurotransmitter. It appears to be active when given orally and readily passes the blood-brain barrier. IDROCILAMIDE & RILUZOLE - CORRECT ANSWER-New agents for the treatment of amyotrophic lateral sclerosis that appear to have spasm- reducing effects, possibly by inhibiting glutamatergic transmission in the CNS. B. DRUGS THAT ACT ON THE SKELETAL MUSCLE - CORRECT ANSWER-... DANTROLENE - CORRECT ANSWER-DANTROLENE Dantrolene interferes with the release of Ca2+ by binding to the ryanodine receptor in the SR of skeletal muscle. Cardiac muscle and smooth muscle are depressed only slightly. Adverse effects include generalized muscle weakness, sedation, and occasionally hepatitis. Dantrolene is also used in malignant hyperthermia. Given IV for this condition BOTULINUM TOXIN - CORRECT ANSWER-Botulinum toxin, injected locally into muscles, is used to treat a form of persistent and disabling eyelid spasm (blepharospasm), as well as other types of local muscle spasm. Local injection of botulinum toxin has become popular for treatment of generalized spastic disorders, e.g., cerebral palsy. DRUGS USED FOR ACUTE LOCAL MUSCLE SPASM - CORRECT ANSWER-A large number of drugs are used for relief of acute temporary muscle spasm caused by local trauma or strain. Most act as sedative or at the level of the spinal cord or brain stem. Cyclobenzaprine may be regarded as the prototype of the group. It is structurally related to the TCAs and has some properties in common with them, e.g. antimuscarinic effects. It is thought to act at the level of the brain stem. It is ineffective in muscle spasm due to cerebral palsy or spinal cord injury. It has strong antimuscarinic actions and causes significant sedation in most patients and confusion and transient visual hallucinations in some. Cyclobenzaprine is indicated for relief of muscle spasm associated with acute, painful musculoskeletal conditions. Primary suture line - CORRECT ANSWER-main suture that approximates the wound edges for first intention healing to occur continuous or running suture - CORRECT ANSWER-a primary suture line consisting of a single strand of suture placed as a series of stitches often used for closure of long incisions "Following" or "running" suture - CORRECT ANSWER-the STSR holds the lower quarter of the suture taut and away from the area of closure; keeps tension on the suture line and keeps it out of the surgeon's line of view continuous sutures should not be used - CORRECT ANSWER-to close tissues that are under a lot of tension interrupted suture line - CORRECT ANSWER-used to close tissues under tension and to close infected tissues; interrupts the pathway of the bacteria localizing the area of infection to a smaller part of the wound traction sutures - CORRECT ANSWER-used to retract a structure that may not be easily retracted with a conventional retractor instrument; a nonabsorbable suture is placed into or around the structure and the suture ends are clamped with a hemostatic clamp; the structure is then pulled to the side of the operative site drawstring or pursestring suture - CORRECT ANSWER-placed in a circular fashion around a structure in such a way that pulling on the suture ends tightens and closes an opening secondary suture line - CORRECT ANSWER-sutures placed to support and ease the tension on the primary suture line, thus reinforcing the wound closure and obliterating any dead spaces retention sutures - CORRECT ANSWER-large-gauge, interrupted, nonabsorbable sutures placed lateral to a primary suture line for wound reinforcement Bridges - CORRECT ANSWER-plastic devices that bridge the closed incision Bolsters - CORRECT ANSWER-pieces of plastic or rubber tubing threaded over the retention suture ends before the ends are tied; once tied they cover retention sutures and prevent them from cutting into the skin Buttonholes - CORRECT ANSWER-holes through which tendon sutures are pulled through and tied over a button to prevent tissue damage Split lead shots - CORRECT ANSWER-may be clamped onto the ends of subcuticular sutures after skin closure umbilical tape - CORRECT ANSWER-used for retraction and isolation of bowel, nerves, vessels, or ducts; used moist vessel loops - CORRECT ANSWER-thin strips made of silicone that can be placed around a vessel, nerve, or duct for the purposes of retracting or isolating; the loops are colored for easy identification of the retracted structures white and yellow loops - CORRECT ANSWER-for nerves and ducts red loops - CORRECT ANSWER-for arteries blue loops - CORRECT ANSWER-for veins Skin closure tapes - CORRECT ANSWER-adhesive-backed strips of nylon or polypropylene tapes used to reinforce a subcuticular skin closure to approximate wound edges of small incisions or superficial lacerations when sutures may not be necessary Skin adhesive - CORRECT ANSWER-a sterile liquid that is applied topically; used on the surface of a wound that will not be under tension in place of adhesive skin closure tapes, staples, or suture How are Anesthesia codes grouped and where can they be found - CORRECT ANSWER-Grouped anatomically, beginning with the head. To find, either use Index / Anesthesia to locate the anatomic area or turn to blue edged Anesthesia 000100 pages. Guidelines are at front of blue chapter. What is a "crosswalk" book - CORRECT ANSWER-Books available to coders to assist by "crosswalking" the known surgical code to an appropriate anesthesia code. BUV - CORRECT ANSWER-Base unit value. What are the 3 different types of anesthesia - CORRECT ANSWER-General, Regional, and Monitored Anesthesia Care (MAC) What is general anesthesia - CORRECT ANSWER-A drug-induced loss of consciousness. Where the patient is unconscious and has no control of their airway. What is regional anesthesia - CORRECT ANSWER-Includes blocks, spinals, and epidurals. A loss of sensation in a region of the body such as: Spinal Anesthesia: An anesthetic agent is injected in the subarachnoid space into the cerebral spinal fluid (CFS) in the patient's spinal canal for surgeries performed below the upper abdomen. Epidural Anesthesia: An anesthetic agent is injected in the epidural space. A small catheter may be placed for a continuous epidural. An epidural can also remain in place after surgery to assist with postoperative pain. Nerve Block: An anesthetic agent is injected directly into the area around a nerve to block sensation for the region the surgery is being performed. Commonly used for procedures on the arms or legs. What is Monitored Anesthesia Care - CORRECT ANSWER-MAC. Anesthesia service where the patient is under light sedation or no sedation while undergoing surgery with local anesthesia provided by the surgeon. The patient can respond to purposeful stimulation and can maintain his airway. The service is monitored by an anesthesia provider who is prepared at all times to convert MAC to general anesthesia if necessary. For MAC, the patient has a decreasedawareness and he or she cannot easily be aroused, but will respond to painful or repeated stimuli. They are not totally unconscious and they are able to control their airway. Local anesthesia - CORRECT ANSWER-is used for minor surgeries. For local anesthesia, the services are included in the CPT® code for the surgical encounter. There would not be a separate code for anesthesia services. Anesthesiologist - CORRECT ANSWER-A physician licensed to practice medicine and has completed an accredited anesthesiology program. These physicians may personally perform, medically direct, or medically supervise members of an anesthesia care team.