Induction Agents - quiz 2 Flashcards
1
Q
Where is site of action of medications?
A
receptor site on the neurons
2
Q
Is GABA inhibitory or excitatory?
A
inhibitory
3
Q
Is glutamate inhibitory or excitatory?
A
excitatory
4
Q
GABA has _____ subunits and _____ subclasses
A
5 subunits 3 subclasses ( alpha, beta, gamma)
5
Q
Everything besides _______ needs GABA to bind
A
Barbituates
6
Q
GABA is a product of?
A
Glutamate
7
Q
When GABA binds to its receptor, what electrolyte is moving though?
A
Chloride
8
Q
NMDA is inhibitory or excitatory?
A
excitatory
9
Q
Glutamate binds and opens receptors up – positively charged ions travel though, making what happen to the signal?
A
making the signal be sent faster, that is why we want to use an antagonist - to block the excitatory effect instead of enhancing it
10
Q
How does Alpha 2 work?
A
with the negative feedback loop and norepinephrine
11
Q
What is a baroreceptor?
A
pick up pressure changes - send information to CNS and releases natural catecholamine’s
12
Q
What are chemoreceptors?
A
pick up CO2 and O2 concentrations within the blood to say “take a breath”
Barbs and Benzo can block these receptors and have long apneic episodes
13
Q
After single bolus dose, you have how many minutes until effects will wear off
A
9 minutes, so less than 9 minutes to get maintenance meds going
14
Q
Duration of effect for boluses is how long?
A
5-9 minutes
15
Q
What is balanced anesthesia?
A
Use of multiple drugs to achieve goal
- Inhalation agents
- IV induction agents
- Sedative/hypnotic agents
- Opioids
- Neuromuscular blocking drugs
16
Q
IV induction agents are all what?
A
Lipophilic
aka non-ionized/lipophilic/hydrophobic
17
Q
The first place IV meds will go is?
A
highly perfused organs (brain, heart, lung)
18
Q
Recovery from a single IV inductions dose is from what?
A
REDISTRIBUTION into more fatty tissue
All drugs used for induction have a similar duration of action after a single dose
19
Q
What is
Compartment 1
Compartment 2
Compartment 3
A
1 - systemic circulation
2 - highly vascular organs
3 - fatty tissues
20
Q
1 compartment model assumes that
A
value of distribution is homogenous from head to toe
After IV injection of the drug, it is restricted to the central blood volume.
21
Q
2 compartment model assumes that
A
after injection, medication distributes to highly vascular organs than to entire body
22
Q
3 compartment model includes
A
medication is distributed though all 3 compartments. Has to be highly lipophilic to get to compartment 3.
Molecule goes in and out of fatty tissues into vasculature until eliminated
23
Q
Context Sensitive half times
A
The longer you give a lipophilic medication to a pt, the more and more and more of it is going to start storing. Because of that you will start to notice a longer half life.
If you are using something that is more lipophilic, as the time increases, the dose should get turned down
e.g. Propofol
24
Q
Barbiturates where created when?
A
In the 30’s - oldest meds we have
over 2000 different barbiturate agents
25
What are the 3 clinical effects we get from barbituates?
Sedative, hypnotic, anticonvulsant
26
Barbituric acid lacks what?
CNS activity.
Hypnotic, sedative and anticonvulsant effects occur through substitutions on the N1, C2, & C5 sites.
27
thiopental has pain with injection due to?
Alkaline (pH >10
28
Why wouldn't Italy ship thiopental to the US
we were using it for lethal injection
29
What is the difference between methohexital and thiopental?
methohexital is ULTRA short acting (otherwise they are the same)
30
What is the MOA of barbiturates?
Post-synaptic enhancement of GABA mediated inhibitory neurotransmitters.
May also have GABA-mimetic effects.
31
Why can barbituates have high rates of overdose?
(GABA mimetic effects) they can activate GABA receptor on own with out help of normal GABA molecule binder.
32
how is barbituates bound?
protein bound
33
Doses for barbiturates are calculated for people with albumin levels 3.5-4.5. What does this mean for people with low albumin levels? e.g. pregnancy, liver disease
increased barbiturate levels and potential for toxicity
34
Barbiturates follow what type of absorption and distribution?
3 compartment model
35
Barbiturates are broken down into what for excretion?
Inactive metabolites
36
Barbiturates cause what during post anesthesia?
significant post anesthesia drowsiness
37
Does barbiturates have any analgesic properties?
no
38
Barbiturates has a decreased effect on what CNS properties?
- Decrease in CMRO2
- Decrease in CBF
- Decrease in ICP and IOP
39
Anesthetic doses or barbiturates have anticonvulsant properties and can do what?
Abruptly stop seizures
40
Cardiovascular effects of barbiturates include
decrease in BP d/t peripheral vasodilation and DECREASED CO.
Rapid injection and large induction doses will have more profound effect in BP
41
Respiratory effects of barbiturates include
- Resp depression
- Decreased minute ventilation
- Laryngospasm, bronchospasm – give lidocaine to blunt spams response
42
Barbiturates cause a decrease in chemoreceptors which cause what?
Decrease in stimulation by CO2 to breathe and Decrease in ventilatory response to hypercapnia and hypoxia.
43
Barbituates and with morphine cause a release of what?
Histamine - When you have histamine releases from certain medications it can compound effects
44
Inadvertent intra-arterial injection of barbiturate can cause
Immediate vasospasm and severe vasoconstriction
treatment is: Dilution of drug by injection of normal saline through failed access site.
45
Treatment of vasospasm d/t intra-arterial injection of a bariturate
papaverine 40-80mcg.
46
Absolute contraindications for administration of barbiturates
allergic reactions and history of porphyria
47
What happens if you give a barbiturate to someone with porphyria?
Excitatory seizures, tachycardia and HTN, abd pain, N/V
| opposite effects of what you would normally see with barbiturates
48
How old are Benzos
Approx 45 years
49
Why are Benzos used in many clinical situation?
Broad scope of properties and low side effect profile
50
What properties do Benzos provide?
Anxiolytic, sedation, anticonvulsant, muscle relation, amnesia
51
What is different about Benzos and barbituates in regards to safety?
Greater margin of safety against overdose
52
Important part of chemical structure with benzos
Benzodiazepine ring
imidazole ring – ring stays closed making it even more lipophilic at physiologic pH
53
Do Benzos need a lipid vehicle?
no
54
In physiologic pH, ______ the diazepine ring closes and midazolam becomes _______.
(>4)
lipophilic
55
Versed onset, peak and duration
Onset 1-5 min
Peak 30 minutes
Duration 2 hours
56
Versed is ______ _______ soluble and _______ ________ bound
lipid soluble
| protein bound
57
Versed is a CYP _______
Substrate
58
How is versed excreted?
Via urinary excretion
59
Despite rapid passage into the brain, midazolam has a
slower effect site equilibrium
60
What is the MOA of versed
Activation of GABA(A) receptor complex and enhancement of GABA mediated chloride currents.
61
Why do we use versed more with induction than other benzo
high reliability, predictable, and effectiveness on GABA A receptors.
62
GABA receptors responsive to benzodiazepines occur almost exclusively on
post-synaptic nerve endings in the CNS
63
Benzos, compared to barbituates, decrease
CMRO2 and CBF
64
Benzos ____________ produces and isoelectric line
CANNOT
65
Benzos produce what in regards to ICP
Little to no change in ICP
66
Benzos have __________ anticonvulsant properties
Potent
67
Versed causes paradoxical excitement in <1 % of pt. What is paradoxical excitement
person not going to sleep – instead greatly agitated
68
Benzos cause a _______ ________ decerase in systemic ___________
Dose Dependent
| blood pressure
69
Post induction hypotension is greater after ___________ then ___________
midazolam than diazepam.
70
Is cardiac output changed with Bezos?
NO
71
What type of amnesia can versed cause?
Anterograde amnesia
72
What happens when you use benzos for sleep aids?
Sleep is not restorative, not hitting REM cycle
73
How long can withdrawal from Benzos last?
Weeks to months
| be careful with giving flumazonal - you can force pt into withdrawal if they have been taking them long term
74
Benzos and barbituates cause significant hyperpolarization, which causes
a global reduction in output in CNS
75
Benzo and barb over dose can cause Respiratory depression, hypotension, coma, confusion. What is your treatment?
Mostly use supportive therapy
76
What is flumazonal?
Benzo antagonist- competitive
77
Why does flumazonal usually need redosed?
Some benzos have longer half lives than flumazemil (ex: midazolam).
200 mcg every 1–2 minutes until the effect is seen, to a maximum of 3 mg per hour
78
What is Remimazolam?
metabolized via esterase instead of by the CYP system in the liver. Esterase is VERY abundant in body so it is rapidly emlimated and has less accumulation
79
What is the most frequently administered drug for induction of anesthesia?
Propofol
| good consistent, predictable sedation
80
Propofol is insoluble, therefor it needs what for emulsification?
lipid vehicle
81
What allergy would prevent you from using propofol?
egg allergy (lipid vehicle has egg protein)
82
Why does propofol need changed every 6 hours?
rate of bacterial growth after 6 hours exponentially increases!!
(increases risk of pts getting infections)
83
Addition of preservatives in propfol inhibits bacterial growth for up to
12 hours
84
What is in the Baxter and Pfizer brands of propofol that is not present in AstraZeneca brands that can lead to an asthma attack?
sulfite
85
Propofol MOA
relatively selective modulator of GABA(A) receptors
86
Onset, peak and duration of Propofol
Onset 30 seconds
Peak
Duration 3-10 minutes
87
In comparing barbs and benzos to propofol, why does propofol have less of a "hangover" effect?
hepatic clearances than just liver (also lungs and biliary system)
88
Propofol is a CPY _______ and _________
Substrate and inhibitor
89
Propofol is ________ during times of focal ischemia
Neuroprotective
90
What might you observe during induction with propofol?
May observe twitching or spontaneous movement (this is NOT seizure activity)
91
Propofol and Benzos both has a profound decrease in systemic blood pressure due to
massive vasodilation
92
Propofol has a dramatic inhibition of what reflex?
Baroreceptor and chemoreceptors
| Profound bradycardia and hypotension in healthy adults
(Decrease ventilatory response to hypoxia and hypercapnia)
93
Propofol causes less laryngospasms than what other med?
Barbituates
94
Is propofol painful on injection?
YES - give 1% lidocaine prior
95
What is a major benefit of propofol in post?
Decreased PONV!
96
Explain propofol infusion syndrome
- lactic acidosis
- Kidney failure, rhabdomyolysis, cardiac arrest
- UNEXPLAINED tachycardia (1st thing you will see)
- Hypertrigyceridemia
97
What is different about Fospropofol in its make up?
Does not require a lipid vehicle, (water soluble prodrug)
98
If Fospropofol can have less "bad" effects on the body, why is it not used more?
Unpredictable onset of action -(Longer than propofol), have to wait for metabolism to occur
People liked the shorter duration and less hangover of propofol
causes more itching
99
Ketamine causes what type of anesthesia?
dissociative
100
Katamine causes a dissociation between what systems?
between thalamocortical and limbic system
101
What type of state will the pt be in when they have been given ketamine?
cataleptic state with eyes open and slow nystagmic gaze
noncomunicative
102
Ketamine can cause delirium, but how do you have to treat it?
Don’t treat delirium when its happening, you CAN pretreat for it prophylactically
103
Does ketamine help with pain?
YES, good analgesic effect (reduces opiate use up to 50%)
104
In regard to chemical structure, ketamine has a racemic mixture. What does this mean?
Ketamine is a mix of S and R antiomeres.
| S more potent than R, AND less psych side effects.
105
what is different with Ketamine in regards to protein binding than barbituates, Benzos and Propofol?
Ketamine is NOT significantly bound to protein
| low albumin levels - burn pts, kidney failure, malnutrition - leads to toxic levels of ketamine
106
In metabolism of Ketamine, what is different about its metabolite in comparison to barbs, benzos and propofol?
it has ACTIVE metabolites with 1/3rd -1/5th potency of ketamine
Active metabolite**– becomes a problem when you have someone with kidney failure (begins to build up)
107
Ketamine onset, peak and duration
Onset - 30-60 seconds
Peak 1 min
Duration 8-10 minutes (up to 25 min if IM)
108
How do you administer ketamine?
slowly, over 60 seconds
109
What is the MOA for ketamine?
NMDA receptor antagonist
| Exerts weak action at GABA(A) receptor.
110
Ketamine is a cerebral vasodilator, which increases?
CBF and CMRO2
NOT recommended for its with intracranial pathology
111
How does ketamine cause sedation?
by blocking excitatory effects
112
What kind of movement may you see on injection of ketamine?
Myoclonic movements
113
Katamine has Centrally mediated sympathetic stimulation which causes an increase in
BP, HR and CO
increased CO gives way to increased CVP
114
What is the effect of ketamine on the respiratory system?
No significant respiratory depression
115
What are some emergence reactions from ketamine?
Vivid dreams, extracorporeal experiences, hallucinations
