NBCRNA CERTIFICATION UPDATED EXAM SCRIPT
QUESTIONS AND SOLUTIONS RATED A+
✔✔Downsides of lighted stylet for intubation? - ✔✔not used in can't ventilate/can't
intubate scenario
more difficult in pt with short thick neck
blind technique: don't use in presence of tumor, foreign body or airway injury
✔✔For using the Trachlight in pediatrics, what should be done when compared for use
in adults? - ✔✔It should be bent at a less acute angle
transillumination will occur sooner
glow more prominent
more false positive results
In adult, should be bent at 90 degrees
✔✔Absolute contraindication to cricothyroidectomy? - ✔✔age < 10, use percutaneous
transtracheal jet ventilation
✔✔Best ways to intubate with limited neck ROM? - ✔✔FOB
blind nasal intubation
✔✔Contraindications to retrograde intubation: - ✔✔neck flexion deformity
obesity or goiter
coagulopathy
pre tracheal abscess
tracheal stenosis
✔✔DLT cuff pressures:
tracheal
bronchial - ✔✔tracheal 5-10 ml
bronchial 1-2 ml (low volume high pressure) - keep deflated if you don't need lung
separation
✔✔Signal transduction order: - ✔✔1st messenger
G-protein
Effector organ
2nd messenger
✔✔Using epinephrine, describe signal transduction. - ✔✔- Epi (1st messenger) binds to
the beta-1 receptor (G-protein)
- Beta-1 receptor activates an effector enzyme (adenylate cyclase)
- This effector enzyme activates 2nd messenger (cAMP)
- cAMP initiates phosphorylation run that increase cAMP
- This increases intracellular calcium --> stronger contraction
,-at same time, these phosphorylation runs activate Ca/ATPase on SR, which increases
lusitropy by enhancing calcium uptake back into the SR
*this is how epic simultaneously improves contractility AND relaxation!
✔✔Signal transduction with the alpha-1 receptor?
What are some other receptors that behave this way? - ✔✔1st messenger: epi/NE
Receptor: alpha 1
Effector enzyme: phospholipase C
2nd messenger: IP3, DAG, Ca2+
Vasopressin-1, histamine-1, muscarinic-1 and 3
✔✔What enzyme deactivates cAMP?
What does it hydrolyze it to? - ✔✔phosphodiesterase
hydrolyzes cAMP to AMP. This turns off the protein kinases and instructs the cell to stop
that specific function
✔✔What do phosphodiesterase inhibitors do to cAMP?
in regards to B-1 and B-2 what do PDEI's do? - ✔✔increase
by turning "off" a mechanism
B-1: increase intracellular calcium and increase isotropy
B-2: decrease intracellular calcium and cause vasodilation
✔✔Stimulation of which muscarinic receptor inhibits adenylate cyclase? - ✔✔M2
✔✔how many subtypes of muscarinic receptor?
Which affect adenylate cyclase and phospholipase? - ✔✔5 subtypes
Even numbered receptors (2&4) inhibit adenylate cyclase
Odd numbered (1,3,5) stimulate phospholipase
✔✔Match each enzyme with its primary function in catecholamine synthesis:
phenylethanolamine N-methyltransferase
Tyrosine hydroxylase
DOPA decarboxylase
Dopamine beta-hydroxylase
What is the rate-limiting step? - ✔✔Tyrosine hydroxylase --> converts tyrosine to DOPA
**RATE LIMITING STEP** TYROSINE HYDROXYLASE
,DOPA decarboxylase --> DOPA to dopamine
Dopamine beta-hydroxylase --> dopamine to NE
phenylethanolamine N-methyltransferase --> NE to Epi
✔✔Each receptor with physiologic action:
B-1
M-3
B-2
M-2 - ✔✔B-1: increased inotropy
M-3: bronchial constriction
B-2: bronchial relaxation
M-2: decreased chronotropy
✔✔Functions carried out by the alpha-1 receptor: - ✔✔Mydriasis
Uterine contraction
arterial constriction
decreased GI motility/tone
contracted sphincters
glycogenolysis
lipolysis
increased sweat gland secretion
✔✔Functions carried out by the B-2 receptor: - ✔✔relaxed detrusor muscle in the
bladder
- stimulates beta cells of pancreas to release insulin
✔✔NE can stimulate its own release by agonizing: - ✔✔presynaptic beta-2 receptor
*presynaptic b-2 increases NE release (+ feedback)
+presynaptic a-2 decreases NE release (- feedback)
✔✔What most accurately describes beta agonist activity? - ✔✔B-1 and 2 agonists
increase cAMP, by turning on adenylate cyclase
B-2 stimulation reduces K+ by activating Na/K pump
- more sensitive to epi than NE
✔✔Where is the greatest % of exogenously administered NE metabolized? - ✔✔liver
kidneys
*by MAO/COMT
- longer DoA
✔✔Termination of action of Endogenous NE is primarily d/t?
, secondary mechanisms? - ✔✔reuptake into the presynaptic neuron
secondary mechanisms:
- deamination by MAO in the synaptic cleft
- diffusion into the bloodstream and degraded by MAO and COMT in the liver and
kidney
✔✔Describe the architecture of the SNS: - ✔✔ACh = NT of SNS ganglia
Cell bodies reside T1-L3 (thoracolumbar)
SNS axons exit the spinal cord via the VENTRAL root
preganglionic fibers: short B fibers, myelinated
postganglionic fibers: long C fibers, unmyelinated
Post:Preganglionic fiber ratio 30:1
✔✔Describe the architecture of the PNS: - ✔✔ACh = NT @ PNS ganglia
cell bodies arise from S2-S4, craniosacral CN 3,7,9,10
Preganglionic fibers: long myelinated B fibers
Postganglionic fibers: short unmyelinated C fibers
Post:Preganglionic fiber ratio 3:1
✔✔Bainbridge reflex is associated with:
What is its purpose? - ✔✔increased preload
tachycardia
It's purpose is to reduce venous congestion and improve forward flow through the heart.
Increased right atrial pressure stretches baroreceptors in the right heart and vagal
afferents transmit this information to the vasomotor center in the medulla. This reduces
PNS tone to the heart, which = increased HR. Stretching of the SA node itself alters its
rate of spontaneous depolarization, which also contributes to an increased HR
✔✔Bezold-Jarisch reflex - ✔✔causes a paradoxical slowing of the HR in response to a
round reduction in venous return, the heart slows to allow adequate fill time.
✔✔Cushing reflex: - ✔✔hypertension
bradycardia
irregular respirations
✔✔Chemoreceptor reflex - ✔✔stimulated by hypoxia and hypercarbia
Increases MV and SNS tone
✔✔Shy drager syndrome causes?
s/sx - ✔✔autonomic dysfunction and degeneration of:
QUESTIONS AND SOLUTIONS RATED A+
✔✔Downsides of lighted stylet for intubation? - ✔✔not used in can't ventilate/can't
intubate scenario
more difficult in pt with short thick neck
blind technique: don't use in presence of tumor, foreign body or airway injury
✔✔For using the Trachlight in pediatrics, what should be done when compared for use
in adults? - ✔✔It should be bent at a less acute angle
transillumination will occur sooner
glow more prominent
more false positive results
In adult, should be bent at 90 degrees
✔✔Absolute contraindication to cricothyroidectomy? - ✔✔age < 10, use percutaneous
transtracheal jet ventilation
✔✔Best ways to intubate with limited neck ROM? - ✔✔FOB
blind nasal intubation
✔✔Contraindications to retrograde intubation: - ✔✔neck flexion deformity
obesity or goiter
coagulopathy
pre tracheal abscess
tracheal stenosis
✔✔DLT cuff pressures:
tracheal
bronchial - ✔✔tracheal 5-10 ml
bronchial 1-2 ml (low volume high pressure) - keep deflated if you don't need lung
separation
✔✔Signal transduction order: - ✔✔1st messenger
G-protein
Effector organ
2nd messenger
✔✔Using epinephrine, describe signal transduction. - ✔✔- Epi (1st messenger) binds to
the beta-1 receptor (G-protein)
- Beta-1 receptor activates an effector enzyme (adenylate cyclase)
- This effector enzyme activates 2nd messenger (cAMP)
- cAMP initiates phosphorylation run that increase cAMP
- This increases intracellular calcium --> stronger contraction
,-at same time, these phosphorylation runs activate Ca/ATPase on SR, which increases
lusitropy by enhancing calcium uptake back into the SR
*this is how epic simultaneously improves contractility AND relaxation!
✔✔Signal transduction with the alpha-1 receptor?
What are some other receptors that behave this way? - ✔✔1st messenger: epi/NE
Receptor: alpha 1
Effector enzyme: phospholipase C
2nd messenger: IP3, DAG, Ca2+
Vasopressin-1, histamine-1, muscarinic-1 and 3
✔✔What enzyme deactivates cAMP?
What does it hydrolyze it to? - ✔✔phosphodiesterase
hydrolyzes cAMP to AMP. This turns off the protein kinases and instructs the cell to stop
that specific function
✔✔What do phosphodiesterase inhibitors do to cAMP?
in regards to B-1 and B-2 what do PDEI's do? - ✔✔increase
by turning "off" a mechanism
B-1: increase intracellular calcium and increase isotropy
B-2: decrease intracellular calcium and cause vasodilation
✔✔Stimulation of which muscarinic receptor inhibits adenylate cyclase? - ✔✔M2
✔✔how many subtypes of muscarinic receptor?
Which affect adenylate cyclase and phospholipase? - ✔✔5 subtypes
Even numbered receptors (2&4) inhibit adenylate cyclase
Odd numbered (1,3,5) stimulate phospholipase
✔✔Match each enzyme with its primary function in catecholamine synthesis:
phenylethanolamine N-methyltransferase
Tyrosine hydroxylase
DOPA decarboxylase
Dopamine beta-hydroxylase
What is the rate-limiting step? - ✔✔Tyrosine hydroxylase --> converts tyrosine to DOPA
**RATE LIMITING STEP** TYROSINE HYDROXYLASE
,DOPA decarboxylase --> DOPA to dopamine
Dopamine beta-hydroxylase --> dopamine to NE
phenylethanolamine N-methyltransferase --> NE to Epi
✔✔Each receptor with physiologic action:
B-1
M-3
B-2
M-2 - ✔✔B-1: increased inotropy
M-3: bronchial constriction
B-2: bronchial relaxation
M-2: decreased chronotropy
✔✔Functions carried out by the alpha-1 receptor: - ✔✔Mydriasis
Uterine contraction
arterial constriction
decreased GI motility/tone
contracted sphincters
glycogenolysis
lipolysis
increased sweat gland secretion
✔✔Functions carried out by the B-2 receptor: - ✔✔relaxed detrusor muscle in the
bladder
- stimulates beta cells of pancreas to release insulin
✔✔NE can stimulate its own release by agonizing: - ✔✔presynaptic beta-2 receptor
*presynaptic b-2 increases NE release (+ feedback)
+presynaptic a-2 decreases NE release (- feedback)
✔✔What most accurately describes beta agonist activity? - ✔✔B-1 and 2 agonists
increase cAMP, by turning on adenylate cyclase
B-2 stimulation reduces K+ by activating Na/K pump
- more sensitive to epi than NE
✔✔Where is the greatest % of exogenously administered NE metabolized? - ✔✔liver
kidneys
*by MAO/COMT
- longer DoA
✔✔Termination of action of Endogenous NE is primarily d/t?
, secondary mechanisms? - ✔✔reuptake into the presynaptic neuron
secondary mechanisms:
- deamination by MAO in the synaptic cleft
- diffusion into the bloodstream and degraded by MAO and COMT in the liver and
kidney
✔✔Describe the architecture of the SNS: - ✔✔ACh = NT of SNS ganglia
Cell bodies reside T1-L3 (thoracolumbar)
SNS axons exit the spinal cord via the VENTRAL root
preganglionic fibers: short B fibers, myelinated
postganglionic fibers: long C fibers, unmyelinated
Post:Preganglionic fiber ratio 30:1
✔✔Describe the architecture of the PNS: - ✔✔ACh = NT @ PNS ganglia
cell bodies arise from S2-S4, craniosacral CN 3,7,9,10
Preganglionic fibers: long myelinated B fibers
Postganglionic fibers: short unmyelinated C fibers
Post:Preganglionic fiber ratio 3:1
✔✔Bainbridge reflex is associated with:
What is its purpose? - ✔✔increased preload
tachycardia
It's purpose is to reduce venous congestion and improve forward flow through the heart.
Increased right atrial pressure stretches baroreceptors in the right heart and vagal
afferents transmit this information to the vasomotor center in the medulla. This reduces
PNS tone to the heart, which = increased HR. Stretching of the SA node itself alters its
rate of spontaneous depolarization, which also contributes to an increased HR
✔✔Bezold-Jarisch reflex - ✔✔causes a paradoxical slowing of the HR in response to a
round reduction in venous return, the heart slows to allow adequate fill time.
✔✔Cushing reflex: - ✔✔hypertension
bradycardia
irregular respirations
✔✔Chemoreceptor reflex - ✔✔stimulated by hypoxia and hypercarbia
Increases MV and SNS tone
✔✔Shy drager syndrome causes?
s/sx - ✔✔autonomic dysfunction and degeneration of:
