EX
B✔
Codeine is a Schedule V drug
Levophanol, Oxycodone, and Hydrocodone areSchedule II drugs
Hydrocodone recently change from ScheduleIII to II drug October 2014.
DX
.B? 4 is true as well
Dextromathorphan is an NMDA antagonist. – Dextromethorphan is an antitussive found in many cough medications
BX
A✔
Methadone unlike morphine is metabolized through N-demethylation by the liver cytochrome P-450 enzyme (CYP1A2), caution in patients receiving multiple medications, specifically antivirals and antibiotics.
Excreted exclusively in the feces and can be given in patient with renal dysfunction
a. 1,2,3 only
b. 1,3 only
c. 2,4 only
d. 4 only
e. All are correct
EX
A✔
Opioids have been proposed to inhibit neurotransmitter release by inhibiting calcium entry, by enhancing outward movement of potassium ions, or by inhibiting adenylate cyclase (AC), the enzyme which converts adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP).
DX
C✔?
CX
D✔
A✔
A✔
B✔
C
D?
D✔
E?
E✔
BX
bioavailability of opioids in the cerebrospinal fluid and epidural space is determined primarily by their hydrophobicity, with less hydrophobic drugs having greater bioavailability.
AX
a. 1,2,3 only
b. 1,3 only
c. 2,4 only
d. 4 only
e. All are correct
C X
AX
B✔
EX
C✔
Bone lesions and hypercalcemia (high blood calcium levels) are also often encountered.
Diagnostic Criteria
Clonal plasma cells >10% on bone marrow biopsy or (in any quantity) in a biopsy from other tissues (plasmacytoma)
A monoclonal protein (paraprotein) in either serum or urine (except in cases of true non-secretory myeloma)
Evidence of end-organ damage felt related to the plasma cell disorder (related organ or tissue impairment, ROTI, commonly referred to by the acronym “CRAB”):
HyperCalcemia (corrected calcium >2.75 mmol/L)
Renal insufficiency attributable to myeloma
Anemia (hemoglobin
BX
E✔
E?
C✔
B?
E ✔?
19. Based on the current thinking about the mechanism of facilitated processing (for example, windup or the "2nd phase of the formation test"), which of the following agents would block the facilitation, but not the primary excitation or first phase? Clonidine (an alpha 1 agonist ) Ibuprofen (a cyclooxygenase inhibitor) L-NAME (a nitric oxide synthetase inhibitor) MK- 801 (an NMDA receptor anatgonist) Morphine (a mu receptor agonist opioid) a. Clonidine, Ibuprofen, L-Name b. Ibuprofen, L-Name, MK-801 c. L-Name, MK 801, Morphine d. Clonidine, MK 801, Morphine e. L-Name, MK 801, Morphine
DX
MK-801 L-Name, Clonidine morphine L- NAME
E X
The first major mechanistic insight was that the induction and maintenance of acute activity-dependent central sensitization was dependent on NMDA receptors,379 revealing a key involvement of glutamate and its receptors
A. Follow and peripheral nerve injury, there is sprouting of postganglionic sympathetic if efferent into the dorsal root ganglia and into the Neuroma.
B. While injury may cause sympathetic terminal to sprout, there is no physiological evidence that such sprouting affects the spontaneous activity of injured afferents.
C. Injury leads to an increase in sympathetic terminal activity, and this increase in circulating catecholamines accounts for the increased sensory terminal activity
D. Sympathetic blockade actually serves to block transmission in the sympathetic afferent the travels with the sympathetic efferents. It is a blockade of a transmission in these afferent that is in fact accounts for the observed pain relief produced, for example by regional sympathectomies.
E. Peripheral injury lead to an increased sympathetic innervation of spinal dorsal horn, neurons leading to a facilitation of their response to otherwise innocuous stimulation.
D?
A/E ✔?
The key question is how and where does the sympathetic nervous system become coupled to the sensory nervous system to produce the pain observed in the clinical situation? The basic observation must be that activity in the sympathetic nervous system initiates abnormal impulse traffic in sensory neurones that leads to pain perception.
numerous studies demonstrating that peripheral nerve injury leads to sympathetic sprouting in the DRG
D ?
C✔
Understanding of the peripheral and central mechanisms of the mechanical allodynia has been perceived as follows:
1) increased excitability of peripheral and central terminals and their cell bodies, including local paracrine mechanisms; 2) The reduction in inhibition (disinhibition) in the spinal cord (i.e. the decreased inhibitory activity of GABA/glycinergic interneurons;
3) The reorganization of synaptic connections in the spinal dorsal horn (Aβ-afferents sprout into the superficial layer
The allodynia and hyperalgesia associated with neuropathic pain may be best explained by:
1) the development of spontaneous activity of afferent input 2) the sprouting of large primary efferents (eg. A-beta fibers from lamina 3 into lamina 1 and 2),
3) sprouting of sympathetic efferents into neuromas and dorsal root and ganglion cells,
4) elimination of intrinsic modulatory systems and
5) up regulation of receptors in the dorsal horn which mediate excitatory processes
C ?
D✔
Lazy French Tarts Sit Nakedly In Anticipation
The order of the nerves passing through the superior orbital fissure from superior to inferior:
L: lacrimal nerve
F: frontal nerve (a branch of the ophthalmic nerve)
T: trochlear nerve (CN IV)
S: superior division of the oculomotor nerve (CN III)
N: nasociliary nerve (a branch of the ophthalmic nerve)
I: inferior division of the oculomotor nerve (CN III)
A: abducens nerve (CN VI)
E ?
D✔