NCE part 2 Flashcards
1
Q
Type A nerve fibers - describe their myelination
A
heavy
2
Q
Type B nerve fiber describe their myelination
A
light myelination
3
Q
type c nerve fibers- describe their myelination
A
no myelination
4
Q
what is type A alpha nerve fiber responsible for
A
proprioception
motor
5
Q
what is type a gamma nerve fiber responsible for
A
muscle spindles
gaMMa - “M’s for Muscles”
6
Q
type a delta nerve fiber is responsible for
A
pain
temperature
“DELToid Pain”
7
Q
type a beta nerve fibers is responsible for
A
touch
pressure
“make a BET!” –>and slam your hand down!!
8
Q
A- gamma nerve is responsible for
A
Muscle Spindles - think muscle tone
9
Q
A-delta nerve fibers are responsible for :
A
Pain and Temperature
10
Q
Which nerve fibers are preganglionic autonomic ?
A
Type B nerve fibers
11
Q
C fibers are responsible for 1) _____via the dorsal root and are _______
A
Pain via dorsal root
and are
Postganglionic Sympathetic fibers
12
Q
Which fiber is responsible for pain via the dorsal root ?
A
C fibers
13
Q
Those are Postganglionic sympathetic nerve fibers .
A
C fibers
14
Q
1 cause of methemoglobinemia
A
Benzocaine
15
Q
Describe Zero Order kinetics . What are drug examples ?
A
1)Constant AMOUNT of drug eliminated per unit of time
2) Metabolic pathways are saturated
Drug ex: Salicylate, theophylline , phenytoin , and ethanol .
16
Q
What is First Order kinetics? Which examples of drugs ?
A
1) Constant FRACTION of drug eliminated per unit of time
2) Elimination proportionate to amount of drug in the body
Drug ex: Most drugs are first order kinetics – SUX
17
Q
Volume distribution
A
Amount of drug in body divided by amount in the in the blood
drug in body/drug in blood
Large Vd= lipid solubility
Small Vd= lipid insolubility
18
Q
What is clearance ?
A
Complete drug removal from a volume of plasma per unit of time.
19
Q
Elimination half time is : Time to eliminate 100% of drug from the plasma . True or False
A
False !
50% ( half)
20
Q
4 half lives =
A
94% complete
21
Q
Context - Sensitive Half-time :
A
Time needed for the plasma drug concentration to decrease by 50% (or any other percentage ) AFTER DISCONTINUING a continuous infusion with a specific duration .
Context = infusion duration
It considers combined effect of : distribution + metabolism+ duration of a continuous IV administration on the drug’s pharmacokinetics
22
Q
A drug that is eliminated by first order kinetics has a half-life of elimination of 6 hours. How much drug remains after 18 hours if 10mg is administered
A
1.25mg
23
Q
160 mg of drug is administered and 20 mg remains 30 hours later. How much drug is lost in the next 20 hours if the drug is eliminated by first order kinetics:
A
15 mg
at third 1/2Life = 20mg
4th = 20/2 = 10mg
5th = 10/2 = 5mg
in the next 20 hours you add the 4th and 5th 1/2 lives b/c they’re each 10 hours = this gives you 15mg of drug lost in the “next 20 hours”
24
Q
mu2
A
Analgesia (Spinal)
Respiratory depression(decrease sensitivity of resp. center to CO2)
Addiction
Constipation (marked) decrease motility and tone of GI muscles
increase CSF pressure (cerebral edema) C/I in head injury
25
kappa
Analgesia (Spinal & Supraspinal)
Dysphoria
Low abuse
Potential
Miosis
Diuresis
26
delta
Analgesia (Spinal & Supraspinal)
Respiratory depression
Physical dependence
Constipation (mild)
27
what type of compound is neuromuscular blocker
quaternary ammonium compound
28
all neuromuscular blockers are structurally related to
acetylcholine
29
T?F
| majority of NMBD are synthetic alkaloids
true
30
NMBD classified by chemical class:
Steroidal
Benzylisoquinoinium
Other
31
H-2 Blockers: name 3 of them
Cimetidine
Ranitidine
Famotidine
32
H-2 Blockers moa
H-2 Blockers: Blocks acid stimulating effects of histamine and ACh
33
Anti-Muscarinic Effect:
Scopolamine is a high affinity muscarinic antagonist
34
Substance P
Neurokinin 1 Antagonists:
35
substance p
Aprepitant: Only PO
Fosprepitant: IV is available
** fun fact: Fosaprepitant is an antiemetic drug, administered intravenously. It is a prodrug of aprepitant
36
name Serotonin Antagonists:
| we use
ondanestron
37
Anti-Histaminergic:
Diphenhydramine: Both antihistamine and anticholinergic effects:
38
Anti-Cholinergic:
| what may be useful in neuraxial induced n/v
Glycopyrrolate may be useful in neuraxial induced N/V
39
Antidopaminergics:
Butyrophenones: Droperidol
Phenothiazines: Prochlorperazine
Benzamines: Metoclopramide
40
Chemotactic Trigger Zone (CTZ)- where is this found
4th ventricle of the brain (located on the floor)
41
name the 5 receptors found in the CTZ that cause n/v
```
Dopaminergic
Serotonergic
Histaminic
Muscarinic
Substance P
```
42
what MAC is an HPV inhibitor
1mac of sevo, iso, des
43
what is nitrous affects on HPV
inhibits HPV
44
what is the effect of thoracic epidural on HPV
little or no effect
45
when does thoracic epidural anesthesia have an indirect effect on 02
if hypotension is allowed and a fall in co
46
what is the IV anesthetic effect on HPV
little or no effect
47
volatile anesthetics inhibit HPV in dose dependent fashion. what is the greatest to least for volatile anesthetics
halothane>enflurane>isoflurane/desflurane/sevoflurane
48
older volatiles were potent HPV inhibitors contributing to high incidence of hypoxemia during OLV in the 60's and 70's
just an FYI- nagelhout says its because they were using 2 mac of halothane
49
explain HPV
increase in pulmonary vascular resistance in atelectatic lung area. HPV optimizes overall gas exchange by shifting blood flow to better ventilated areas of the lung
50
what drug has been demonstrated to enhance effects of NO and may blunt rebound pulmonary pressure that occur during weaning off of inhaled NO
sildenafil
51
sildenafil and tadalafil have shown benefits in what chronic condition but not approved for these settings
chronic pulmonary arterial HTN
52
phosphodiesterase 5- (PDE5)- do they have higher expression in pulmonary circulation or systemic circulation
pulmonary circulation
53
due to phosphodiesterase 5 higher expression in pulmonary circulation do they have higher selective effect on PVR or SVR
PVR
54
phosphodiesterase inhibitors prevent the degradation of what two things
cGMP and cAMP
55
when phosphodiesterase inhibitors inhibit the degradation of cGMP and cAMP what activates this two things
NO
56
so when NO activates cGMP and cAMP what does that lead to
vasodilation
57
the vasodilation that results when cGMP and cAMP is activated by NO is through activation of
protein kinases and reduction of cytosolic calcium
58
what type of of phosphodiesterase enzyme inhibitor is milrinone
adenosine 3,5-cAMP selective phosphodiesterase
59
nebulized milrinone leads to a reduction in
relative reduction in PVR compared to SVR
60
Calcium Channel Blockers are particularly successful in treating hypertension in the what three groups
elderly
african american
salt sensitive patients
61
Median Nerve Injury
Ape Hand (unable to oppose Thumb)
62
Ulnar Nerve Injury
claw hand
63
Radial Nerve Injury
wrist drop
64
Axillary Nerve Injury
Inability to abduct arm
65
Musculocutaneous Nerve Injury
Inability to Flex Forearm
66
```
Intravascular infusion of which of the following substances would be most effective in promoting the osmotic movement of water into the circulation from the extracellular space
A.) NaCl
B.) Mannitol
C.) Dextrose
D.) Albumin
```
albumin
67
```
The most potent inhalational anesthetics have
A.) low blood solubility
B.) High blood solubility
C.) Low lipid solubility
D.) High lipid solubility
```
High lipid solubility
68
```
Build up of inhalational anesthetic in the brain is fastest for an agent that has:
A.) low blood solubility
B.) High blood solubility
C.) Low lipid solubility
D.) High lipid solubility
```
A.) low blood solubility
69
How many mg are there in 10 mL of a 4% solution of cocaine
400 mg
| 4% = 40 mg x 10 cc = 400
70
K+ Sparing: works where in the kidney tubes
Distal part of distal convoluted tubule
| Collecting ducts/tubules
71
Carbonic Anhydrase inhibitors: work where in the kidneys
Brush border of proximal tubule
72
Loop: where do they work
loop of henle
73
thiazide: work where
Proximal Part of distal convoluted tubule
74
Osmotic: work where in the kidney
Proximal convoluted tubule
descending limb of loop of henle
distal part of distal convoluted tubule
collecting ducts/tubules
75
plasma cholinesterase production is the work of how many genes?
2 genes
76
what does Dibucaine number of 80 represent
DN = 80 = present on both genes = homozygous (plasma cholinesterase)= Normal
77
dibucaine number of 40-60 represent
DN = 40-60 = only present on one gene = heterozygous (1 in 480) produce 50% of enzyme
78
dibucaine number of 20
DN = 20 = missing on both genes = homozygous (atypical plasma cholinesterase) (1in 3200).
79
Succinylcholine Disadvantages (6)
Myalgia
Hyperkalemia
Cardiac dysrhythmias
MH
Phase II Block: Resembles NMDR (>4 mg/kg)
Second Dose Effect: Brady after close second dose secondary to succinylmonocholine
80
Drugs that interfere with Plasma Cholinesterase:
| 5
1. Organophosphate exposure
2. Anticholinesterase meds
3. Metoclopramide
4. MAOI
5. Oral contraceptives used long-term
81
why is succinylcholine dose 2x ed95
because of its rapid hydrolysis by plasma cholinesterase
82
is succs competitive with Ach
no.
83
are NMDR competitive with ACH
Yes
84
name 5 conditions that interfere with plasma cholinesterase
```
Liver disease (severe)
Chronic renal failure
Starvation
Dialysis (soon after)
Infants (50%) by age 6 (70%), puberty (100%)
```
85
in context of neuromuscular blockers- what is ED50 and ED 95
Measured by the amount of drug necessary to decrease the height of the baseline twitch by 50% and 95%
86
How do we compare the potency of NMDR?
Potency and onset have an inverse relation
low potency = Higher rate of onset
high potency = lower rate of onset
87
low potency NMBD
rapid onset
88
high potency NMBD
slow onset
89
the onset of action of NMBD is inversely proportional to what
potency
90
Molar potency is highly predictive of a dugs time to onset of effect. what drug is the exception to this rule
atracurium
91
molar potency is expressed in what units?
| Why?
micromoles/kg
molecules of drug are VARIABLE
number of nicotinic receptors are FIXED
therefore, the fewer the number of molecules it takes (per kg of body wt) to saturate the receptor, the greater the affinity the drug has (the greater the potency) .
L - does that work for you? or want more? :D
The rationale for expressing potency in moles per kilogram is…[because] ultimately, we have a variable number of molecules chasing a fixed number of nicotinic receptors. The fewer molecules it takes (per kilogram of body weight) to achieve a given degree of receptor occupancy, the greater the affinity the drug has for the receptor. This is best expressed in micromoles per kilogram rather than in milligrams per kilogram.
92
what is the issues with hyperparathyroidism and NMBD
hypercalcemia is associated with decreased sensitivity to atracurium and thus a short duration of neuromuscular blockade
Muscle-nerve models have shown hypercalcemia to decrease sensitivity to tubocurarine and pancuronium
93
why does chronic use of anticonvulsant therapy need an increase dose to NMBD to achieve blockage.
can be attributed to
- increased clearance.
- increased binding of the nueuormuscular blockers to alpha 1 acid glycoproteins
- and/or up regulation of neuromuscular acetylcholine receptors.
94
hypothermia or magnesium sulfate do what to NMBD
potentiates blockade
95
antidysrhythmics such as quinidine do what to NMBD
potentiate NMBD
96
LA given in large doses do what do NMBD
potentiate it
97
high magnesium concentrations do what to calcium channel at the presynaptic nerve terminals
inhibit release of acetylcholine
98
antibiotics can potentiate neuromuscular blockers name 5 of them
```
aminoglycosides
polymyxin
lincomycin
clindamycin
tetracycline
```
99
what is the moa of how antibiotics potentiate neuromuscular blockers
inhibit the prejunctional release of acetylcholine and
| depresses post junctional nicotinic acetylcholine receptor sensitivity to acetylcholine.
100
Inhalation anesthetics potentiate the neuromuscular blocking effect of NMBD
what is the order
DES > SEVO > ISO > Halothane > Nitrous Oxide, barbiturate, or propofol
101
3 Mechanisms for inhalation potentiation of NMBD:
Central effect on alpha motoneurons and interneruonal synapses
Inhibition of postsynaptic nicotinic acetylcholine receptors
Augmentation of antagonist’s affinity at the receptor site
102
roc is how many times less potent than vec
6times
103
roc eliminated by and excreted in
eliminated by liver excreted in bile
104
roc remains stable for how many days at room temperature
60
105
vecuronium is metabolized to
3-OH, 17-OH, 3,17-di-OH
106
why does vecuronium have prolonged neuromuscular blockade with prolonged admnistration
3-oh has 80% the neuromuscular blocking potency and this metabolite will build up and increase the blocking potency of vec
107
duration of vecuronium relies on liver or renal function more
liver function more than renal function
108
pancuronium is it long or short acting. potent or not
potent long acting
109
pancuronium has what two special properties
Vagolytic and butyrylcholinesterase inhibiting properties
110
how long is pancuronium stable for at room temps
6mo
111
accumulation of 3-oh metabolite is responsible for pancuroniums what
prolongation of the duration of action
112
what percent of pancuronium is eliminated by kidneys
40-60%
113
what is the only currently available short acting NMBD
Mivacurium
114
mivacurium is metabolized by
Metabolized by butylcholinesterase at about 70-88% the rate of Sch to a monoester
115
what can be considered problematic if we push mivacurium too fast
May produce histamine release especially if given rapidly
116
name the isomer of astracurium
cisatracurium
117
how is cisatracurium eliminated
hoffman elimination to laudanosine and a mono quaternary alcohol metabolite
118
what percent is hoffman elimination
other ogans
renal
77%
23%
16%
119
how much more potent is cisatracurium than atracurium
4-5x
120
what is the relationship to aludanosine
5 times less laudanosine is produced and is thought one of no clinical consequence
121
does cisatracurium produce histamine release
no
122
Tubocurarine
```
Tubocurarine:
Monoquarternary, long acting
No active metabolism
Excreted unchanged in urine; liver is secondary
Not suitable for renal or liver failure patients
Onset slow
Duration is long
Recovery slow
Intubating dose 0.5 – 0.6 mg/kg
Maintenance dose are 0.1 – 0.2 mg/kg
```
123
Atracurium
Atracurium
Racemic mixture of 10 stereoisomers
Isomers are separated into 3 geometrical isomer groups that are designated cis-cis, cis-trans, and trans-trans
Designed to undergo spontaneous degradation at physiologic temp and pH by Hofmann elimination yielding a laudanosine (tertiary amine) and a monoquaternary acrylate metabolite
Can undergo ester hydrolysis
Hoffmann elimination fragments atricurium to laudanosine and a monoquaternary acrylate
Laudanosine depends on the liver for clearance with ~70% excreted in bile with remainder in the urine
124
slide 15&
16
125
tetracycline potentiates NMBD by exhibiting ONLY what activity
by depressing POST junctional nicotinic acetylcholine receptor sensitivity to acetylcholine ONLY
no inhibition of prejunctional release
