APEX FINAL 1 LATEST 2024 ACTUAL EXAM 1000+ QUESTIONS AND CORRECT DETAILED ANSWERS
Types of nicotinic receptors - (answer) Nn: presynaptic (nerve cell)
Nm: postsynaptic (muscle cell)
Postsynaptic Nicotinic Receptors - (answer) Pentameric: 2 alpha, 1 beta, 1 delta, 1 epsilon subunits
Each alpha subunit binds 1 ACh.
Which subunits need to be occupied to open the nicotinic receptor - (answer) alpha and alpha
the channel opens when both are occupied and Na+ & Ca++ flow in, K+ flows out.
Acetylcholinesterase - (answer) Positioned around Nn and Nm nicotinic receptors. Hydrolyzes ACh
almost immediately after binding. Ensure muscle contractions are discreet and not sustained.
Extrajunctional receptors - (answer) Pathologic variant of ACh (nicotinic) receptors that have become
denervated
-resemble receptors present in fetal development = these are replaced by the adult subtype once
innervation takes place
-proliferate after muscle injury/disease/burns
-the alpha 7 receptor is depolarized by both succ and its metabolite choline (choline makes a significant
contribution to hyperkalemia)
Presence of extrajunctional receptors predisposes patients to what? - (answer) Hyperkalemia
Extrajuctional receptors reaction to NDNMB's - (answer) increased resistance = need to use higher
doses
Extrajunctional receptors reaction to succ - (answer) More sensitive - receptors stay open longer (more
K+ leak) = this is why succ can cause hyperkalemia
2 types of extrajunctional receptors (subunit makeup) - (answer) 1- gamma subunit replaces epsilon
subunit
,APEX FINAL 1 LATEST 2024 ACTUAL EXAM 1000+ QUESTIONS AND CORRECT DETAILED ANSWERS
2- 5 alpha subunits
Treatment of succ induced hyperkalemia - (answer) -IV CaCl
-Hyperventilation
-Glucose & Insulin
TOF fade - (answer) caused by antagonism of presynaptic neuron.
-binding of ACh to presynaptic neurons leads to feed-forward release mobilization of more ACh.
NDNMB's bind to the Nn receptor and block ACh from binding.
-Initial stimulation causes release of ACh, but because of the antagonism, a new supply of ACh is not
mobilized and the twitch "fades" out.
presynaptic release of Ach - (answer) 2 supplies of Ach available for release
-Ach available for immediate release
-Ach that must be mobilized b/f release = presynaptic binding of Ach causes Ca++ channels to open and
increased intracellular Ca++ which destabilizes the proteins that hold the Ach vesicles in places allowing
for exocytosis
What is the defining mechanism of fade - (answer) the presynaptic Ach receptor. If new Ach is not
mobilized through this mechanism the muscle contraction fades
feed forward action of Ach - (answer) some of the Ach released into the synaptic cleft binds to the
presynaptic receptor perpetuating release.
How does succinylcholine work? - (answer) binds to the nicotinic receptors on the motor endplate
causing them to depolarize but because it is not hydrolyzed by acetylcholine esterase, the muscle stays
contracted causing a paralysis.
Molecular makeup of succinylcholine - (answer) Ach molecules joined together - this makeup is the
basis for many of Succ side effects. This what Ach does throughout the body
,APEX FINAL 1 LATEST 2024 ACTUAL EXAM 1000+ QUESTIONS AND CORRECT DETAILED ANSWERS
Why Succinycholine does not cause fade - (answer) -Succ is a Nn agonist so it continually stimulates
the release of ACh. The continued binding of ACh to the postsynaptic receptors leads to initial
fasciculation and then paralysis due to inability of channels to close leading to a state of absolute
refractory.
How long should Succ be avoided after a denervation injury - (answer) for first 24-48h, and for up to 1
year after
(except for burn which Succ should be avoided for several years following)
Acetyltransferase - (answer) enzyme that catalyzes Acetyl CoA and choline
Twitch monitor placement - Onset - (answer) Onset (Intubation)
Muscle: Obicularis Oculi
Function: Closes eyelid
Nerve: Facial
Twitch monitor placement - Recovery - (answer) Emergence (Extubation)
Muscle: Adductor Pollicis or flexor hallucis
Function: Adducts thumb
Nerve: Ulnar or posterior tibial
Phase I vs Phase II block - (answer) Phase I: the absence of fade & post-tetanic potentiation, constant
but diminished response to double burst stimulation (Succ)
Phase II: presence of fade & post-tetanic potentiation (NDNMB)
What distinguishes between a phase 1 and phase 2 block - (answer) the presence or absence of fade
When can succ cause a phase 2 block - (answer) high doses of Succ can cause a phase II block (high IV
bolus or infusion)
, APEX FINAL 1 LATEST 2024 ACTUAL EXAM 1000+ QUESTIONS AND CORRECT DETAILED ANSWERS
Dose > 7-9mg/kg
30-60 min of continuous exposure
Fade with tetany and prolonged duration
Tests for recovery from NMBs - (answer) Tidal vol >5ml/kg: 80% occupied
4/4 twitches, no fade: 70% occupied
Vital capacity > 20mL/kg: 70% occupied
Sustained tetany (50Hz): 60% occupied
double burst stimulation: 60% occupied
Inspiratory force -40cm H20: 50% occupied
Head lift > 5 sec: 50% occupied
Hand grip > 5 sec: 50% occupied
Holding tongue blade against force: 50% occupied
tongue blade is probably best
TOF result that indicates residual muscle neuromuscular blockake - (answer) TOF < 0.9
Succ A/E - (answer) Bradycardia: M2 receptor on SA node) peds and/or 2nd dose
Tachycardia and HTN (more common in adults than bradycardia)
Hyperkalemia: usually transient unless there extrajunctional receptors are present
Increased intraocular pressure (caution w/ open globe injuries)
Increased ICP
Increased intragastric pressure & lower esophageal sphincter tone
Malignant Hyperthermia: Masseter spasm can be first sign - however can also be normal fasciculation so
must correlate w/ other clinical signs
Types of nicotinic receptors - (answer) Nn: presynaptic (nerve cell)
Nm: postsynaptic (muscle cell)
Postsynaptic Nicotinic Receptors - (answer) Pentameric: 2 alpha, 1 beta, 1 delta, 1 epsilon subunits
Each alpha subunit binds 1 ACh.
Which subunits need to be occupied to open the nicotinic receptor - (answer) alpha and alpha
the channel opens when both are occupied and Na+ & Ca++ flow in, K+ flows out.
Acetylcholinesterase - (answer) Positioned around Nn and Nm nicotinic receptors. Hydrolyzes ACh
almost immediately after binding. Ensure muscle contractions are discreet and not sustained.
Extrajunctional receptors - (answer) Pathologic variant of ACh (nicotinic) receptors that have become
denervated
-resemble receptors present in fetal development = these are replaced by the adult subtype once
innervation takes place
-proliferate after muscle injury/disease/burns
-the alpha 7 receptor is depolarized by both succ and its metabolite choline (choline makes a significant
contribution to hyperkalemia)
Presence of extrajunctional receptors predisposes patients to what? - (answer) Hyperkalemia
Extrajuctional receptors reaction to NDNMB's - (answer) increased resistance = need to use higher
doses
Extrajunctional receptors reaction to succ - (answer) More sensitive - receptors stay open longer (more
K+ leak) = this is why succ can cause hyperkalemia
2 types of extrajunctional receptors (subunit makeup) - (answer) 1- gamma subunit replaces epsilon
subunit
,APEX FINAL 1 LATEST 2024 ACTUAL EXAM 1000+ QUESTIONS AND CORRECT DETAILED ANSWERS
2- 5 alpha subunits
Treatment of succ induced hyperkalemia - (answer) -IV CaCl
-Hyperventilation
-Glucose & Insulin
TOF fade - (answer) caused by antagonism of presynaptic neuron.
-binding of ACh to presynaptic neurons leads to feed-forward release mobilization of more ACh.
NDNMB's bind to the Nn receptor and block ACh from binding.
-Initial stimulation causes release of ACh, but because of the antagonism, a new supply of ACh is not
mobilized and the twitch "fades" out.
presynaptic release of Ach - (answer) 2 supplies of Ach available for release
-Ach available for immediate release
-Ach that must be mobilized b/f release = presynaptic binding of Ach causes Ca++ channels to open and
increased intracellular Ca++ which destabilizes the proteins that hold the Ach vesicles in places allowing
for exocytosis
What is the defining mechanism of fade - (answer) the presynaptic Ach receptor. If new Ach is not
mobilized through this mechanism the muscle contraction fades
feed forward action of Ach - (answer) some of the Ach released into the synaptic cleft binds to the
presynaptic receptor perpetuating release.
How does succinylcholine work? - (answer) binds to the nicotinic receptors on the motor endplate
causing them to depolarize but because it is not hydrolyzed by acetylcholine esterase, the muscle stays
contracted causing a paralysis.
Molecular makeup of succinylcholine - (answer) Ach molecules joined together - this makeup is the
basis for many of Succ side effects. This what Ach does throughout the body
,APEX FINAL 1 LATEST 2024 ACTUAL EXAM 1000+ QUESTIONS AND CORRECT DETAILED ANSWERS
Why Succinycholine does not cause fade - (answer) -Succ is a Nn agonist so it continually stimulates
the release of ACh. The continued binding of ACh to the postsynaptic receptors leads to initial
fasciculation and then paralysis due to inability of channels to close leading to a state of absolute
refractory.
How long should Succ be avoided after a denervation injury - (answer) for first 24-48h, and for up to 1
year after
(except for burn which Succ should be avoided for several years following)
Acetyltransferase - (answer) enzyme that catalyzes Acetyl CoA and choline
Twitch monitor placement - Onset - (answer) Onset (Intubation)
Muscle: Obicularis Oculi
Function: Closes eyelid
Nerve: Facial
Twitch monitor placement - Recovery - (answer) Emergence (Extubation)
Muscle: Adductor Pollicis or flexor hallucis
Function: Adducts thumb
Nerve: Ulnar or posterior tibial
Phase I vs Phase II block - (answer) Phase I: the absence of fade & post-tetanic potentiation, constant
but diminished response to double burst stimulation (Succ)
Phase II: presence of fade & post-tetanic potentiation (NDNMB)
What distinguishes between a phase 1 and phase 2 block - (answer) the presence or absence of fade
When can succ cause a phase 2 block - (answer) high doses of Succ can cause a phase II block (high IV
bolus or infusion)
, APEX FINAL 1 LATEST 2024 ACTUAL EXAM 1000+ QUESTIONS AND CORRECT DETAILED ANSWERS
Dose > 7-9mg/kg
30-60 min of continuous exposure
Fade with tetany and prolonged duration
Tests for recovery from NMBs - (answer) Tidal vol >5ml/kg: 80% occupied
4/4 twitches, no fade: 70% occupied
Vital capacity > 20mL/kg: 70% occupied
Sustained tetany (50Hz): 60% occupied
double burst stimulation: 60% occupied
Inspiratory force -40cm H20: 50% occupied
Head lift > 5 sec: 50% occupied
Hand grip > 5 sec: 50% occupied
Holding tongue blade against force: 50% occupied
tongue blade is probably best
TOF result that indicates residual muscle neuromuscular blockake - (answer) TOF < 0.9
Succ A/E - (answer) Bradycardia: M2 receptor on SA node) peds and/or 2nd dose
Tachycardia and HTN (more common in adults than bradycardia)
Hyperkalemia: usually transient unless there extrajunctional receptors are present
Increased intraocular pressure (caution w/ open globe injuries)
Increased ICP
Increased intragastric pressure & lower esophageal sphincter tone
Malignant Hyperthermia: Masseter spasm can be first sign - however can also be normal fasciculation so
must correlate w/ other clinical signs
