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Pharmacology > Quiz 2- IV induction Agents > Flashcards

Quiz 2- IV induction Agents Flashcards

Intro, Barbiturates, Benzodiazepines, Propofol, Ketamine

1
Q

Neurotransmitters are stored in _____ ______, located in the ______ terminal.

A

Synaptic vesicles

Presynaptic or axon

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2
Q

Neurotransmitters are released into the ____ ____ by the presence of _____.

A

Synaptic Cleft

Calcium

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3
Q

Binding of neurotransmitters occurs at the _____ _____, but re-uptake occurs at the _____ ______.

A

Postsynaptic membrane

Presynaptic neuron

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4
Q

True or False: GABA has 1 binding site.

A 
False
GABA has multiple binding sites within it that different drugs bind to:
-benzos
-propofol
-volatile anesthetics
-ethanol
-neurosteroids
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5
Q

What is the precursor to GABA?

A

glutamate

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6
Q

What effect does a GABA agonist have?

A

Inhibitory

-blocks impulses through neuron

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7
Q

Glutamate is an _____ neurotransmitter for the ____ receptor.

A

excitatory

NMDA

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8
Q

How does the Alpha2 receptor negative feedback loop work?

A

Excess norepi in synaptic cleft binds to presynaptic alpha 2 receptors and inhibits release of norepi

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9
Q

What receptor does precedex work on?

Agonst or antagonist?

A

Alpha 2 agonist

dex works as a false norepi

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10
Q

Where are Baroreceptors located & what do they do?

A

Aortic Arch & Carotid Body

Signals travel to medulla and regulate HR, arterial, and venous tone according to MAP

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11
Q

What are Chemoreceptors?

A

detect levels of CO2, O2, and pH in body

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12
Q

Advantages of IV anesthesia/induction agents?

A

1) Provide rapid onset of general anesthesia (30 seconds - 1 minute)
2) Can be used for maintenance phase of general anesthesia
3) Can provide sedation for M.A.C.

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13
Q

How long after induction do emergence symptoms occur?

A

<9 minutes

Need to start maintenance before then!

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14
Q

Disadvantage of IV anesthesia?

So we use ___ anesthesia.

A

There is no 1 med that provides hypnosis, amnesia, analgesia, & immobility

“balanced anesthesia” - multiple drugs to achieve goal

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15
Q

Are IV induction agents hydrophilic or lipophilic?

Ionized or non-ionized?

A

All are lipophilic to penetrate tissues (brain & spinal cord) for rapid onset

Non-ionized= lipophilic

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16
Q

True or False: Single dose termination/recovery after IV induction is determined by metabolism.

A

False!
It’s by redistribution of the drug to less perfused tissues
(vessel rich–> vessel poor group)

All induction drugs have the same duration of action and are not dependent on individual patient metabolism

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17
Q

IV bolus 3 compartment model

What are the 3 compartments?

A

1) Med goes to general circulation (C1)
2) –> distributes to vessel rich organs: brain, liver, kidneys, gut (C2)
3a)–> rapid redistribution to vessel poor group: muscles (shallow)
3b)–> slow distribution to peripheral compartments: fat (deep)
(C3= shallow+deep)
–> metabolism

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18
Q

Name some IV induction agents

A
  • Barbiturates
  • Benzodiazepines
  • Propofol
  • Ketamine
  • Etomidate
  • Dexmedetomidine
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19
Q

Barbiturates type of drug

A

sedative, hypnotic, anticonvulsant

oldest class still available, but not used d/t safety profile

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20
Q

Barbs are derived from barbituric acid, which has effects that occur though ____ on the __ __& __ sites

A

substitutions on the N1, C2, & C5 sites

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21
Q

Which two barbs used in anesthesia occur via substitution at C2?

A

Thiopental & Methohexital

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22
Q

Thiopental and Methohexital have a ___ onset and ___ duration

A

Rapid & Short

10-30 seconds)& (5-10 min

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23
Q

Which barb has myoclonic/excitatory movements with induction bolus?

A

Methohexital

Movements are the body’s natural response to a flood of inhibition/ blunting of sympathetic outflow

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24
Q

Barbiturates Mechanism of Action

A

Post-synaptic enhancement of GABA mediated inhibitory neurotransmitters

May have GABA-mimetic effects

(GABA agonist- inhibitory action to cause profound hyperpolarization)

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25
What are GABA-mimetic effects?
Barbiturates don't need GABA with higher doses as opposed to Benzos
26
Barbiturates (reversibly/irreversibly?) bind to ____ ____.
``` reversibly plasma proteins (albumin) ```
27
What causes a higher unbound fraction of barbiturate, thus causing a greater clinical effect?
1) Decreased plasma protein concentrations - Uremia - Liver disease - 3rd Trimester 2) Competition of other drugs for protein binding sites
28
What drugs compete with Barbiturates, thus increasing the unbound fraction of drug?
1) Aspirin 2) Naproxen 3) Indomethacin 4) Warfarin
29
Barbiturate absorption and distribution follow a __ compartment model
3
30
Barbs ____ metabolites are excreted in the ____.
inactive | urine
31
Barbiturate metabolism is in the ____ and is a ____ system ___.
Liver | CYP450 system inducer
32
CNS effect of barbiturate? Analgesic? Anticonvulsant?
Loss of consciousness in 10-30 seconds (level titratable) NO analgesic effect YES anticonvulsant-can abruptly stop seizures
33
Barbiturate CV effects?
- Mass depression of vasomotor center - ↓BP from vasodilation - Compensatory ↑HR (may make ↓BP transient) *
34
Barbiturate Respiratory effects?
- Depression - ↓response to CO2 - Laryngospasm, bronchospasm!!!!
35
Barbiturates cause a dose dependent release of _____, which causes ____ and ____.
Histamine, which causes vasodilation and hypotension
36
What happens with inadvertent intra-arterial injection of barbiturates?** Treatment?
- immediate vasospasm - severe vasoconstriction - intense pain - blanching of entire extremity - HIGH risk for ischemic gangrene** Treatment: - Dilute with NS flush - Papaverine for vasospasm -Systemic heparinization
37
Absolute contraindication to barbituates
- Hx allergic reaction | - Hx of Porphyria
38
What do NMDA antagonists do?
- Blocks receptor sites of NMDA to slow down propagation of action potential - Stops fight or flight hormones, therefore promote sedation
39
Do barbs or benzos reduce CNS O2 and blood flow more?
Barbs
40
Benzodiazepine Drugs
- Librium - Diazepam - Serax - Lorazepam - Midazolam
41
Benzodiazepine mechanism of action?
- GABA-A agonist - Causes influx of Chloride ions ➞ hyperpolarizes neurons (less excitable) - Midazolam has greater potency & affinity for GABA-A (2-3x> diazepam)
42
What are benzos used for?
Used often- broad scope of properties & low side effect profile - Anxiolytic - Sedation - Anticonvulsant - Muscle relaxation - Amnesia
43
Why are benzos better over barbs?
- Greater margin of safety against overdose*** - Less abuse potential - Fewer/ less sig drug interactions - Do not induce hepatic microsomal enzymes
44
What is special about the chemical structure of Midazolam?
Imidazole ring!
45
Imidazole ring?
Versed Chemical Structure - In solution pH 4: OPEN - pH >4 (body): CLOSES & becomes lipophilic!! Explains rapid onset 1-5min!
46
Versed Pharmacokinetics - CNS onset? - relationship to proteins?
- highly lipid soluble= enters CNS fast, but slow effect at site - highly protein bound
47
Versed metabolism is in the ____ and is a CYP ___.
liver | CYP substrate
48
Benzos are excreted in the ___.
urine
49
Versed CNS effects - (CMRO2) Cerebral Metabolic Rate of O2 and CBF? - EEG? - ICP? - Neuroprotective? - Anti convulsant?
- ↓CNS O2 & blood flow (but less than barbs) - Cannot produce isoelectric EEG - Cannot produce isoelectric EEG - Not neuroprotective - POTENT anticonvulsant properties**
50
Versed CV effects - BP - SVR - CO
- Hypotension d/t vasodilation ↓SVR (versed>diazepam) - CO no change - does not prevent sympathetic response to intubation (↑HR & BP)
51
Versed Respiratory effects
(same as barbs, but lessened) - minimal, dose dependent decreased ventilation - ↓response to CO2 - Synergistic and additive with opioids!!!** may cause apnea*
52
Versed side effects
- allergic rx rare - drowsiness>sedation - Sleep is not restorative* - Anterograde amnesia- alleviates anxiety**
53
Withdrawal of Benzos and Barbs: - Duration? - CNS & CV effects?
- can last weeks-months - CNS: anxiety, insomnia, seizures, coma, agitations, mania, psychosis, suicide - ↑HR, ↑BP, postural hypotension (deaths*)
54
Benzo and Barb overdose: - Causes? - Reversal? - Tx?
- Respiratory depression, hypotension, coma, confusion - Benzo ONLY reversal= flumanizel (caution in chronic users- immediate withdrawal can be = dangerous) - Tx: supportive therapy
55
What is Flumazenil?
- Reversal for benzos - Benzo antagonist- competitive - May require mult. doses - Versed has a longer 1/2 life than it
56
Versed dosing
Healthy adult <60: 1-2.5mg IV over 2 min >60, ill: 1-1.5mg IV over 2 min reduce doses with other sedatives/narcs
57
Remimazolam
- new drug pending - metabolism via esterases (already in blood stream) = more rapid clearance & less accumulation because does't have to make it past 1st compartment
58
Propofol - Use - Chemical structure
- Used for IV maintenance of general anesthesia | - insoluble & requires a lipid vehicle for emulsification**
59
Drawbacks for propofol emulsification
- Supports bacterial growth (6hr) - Allergies - soy & egg (depending on solution) - Asthmatic episodes & sulfite allergic rx in generic
60
Propofol mechanism of action
Works on GABA-A receptors
61
``` Propofol pharmacokinetics: Onset? Duration? Clearance? Compartment model? CYP? ```
- Rapid onset (30 sec) - Rapid duration (3-10 min) with minimal residual CNS effects* - Rapid clearance - 3 compartment model - CYP substrate and inhibitor (irrelevant for 1-time doses)
62
Propofol CNS effects: - CNS O2 & Blood flow? - ICP? - IOP? - Neuroprotective? - Anti-epileptic?
- ↓CNS O2 & blood flow - ↓ICP - ↓IOP - Neuroprotective during focal ischemia** - Anti-epileptic- yes (may cause twitching during induction- not seizure activity)
63
Propofol CV effects: - BP - SVR - HR
- ↓↓BP: vasodilation, ↓SVR, ↓preload | - Inhibition of baroreceptor reflex= ↓HR/BP
64
Propofol Respiratory effects
- potent respiratory depression - apnea after induction - ↓response to O2 & CO2 - ↓↓upper airway reflexes (less spasm risk compared to benzos)
65
Other propofol effects (benefits and SE)
- anti-emetic properties - pain on injection** avoid small hand IV - bradycardia - infection risk - elevated serum triglycerides (longer use) - potential for PE/ pulm edema - antipyretic - antioxidant - propofol infusion syndrome
66
What is propofol infusion syndrome (+adult presentation)?
Lactic Acidosis for use > 48 hrs or 67mcg/kg/min *Sign= Unexpected Tachycardia*** eval for acidosis (BMP/ABG) Can cause kidney failure, rhabdo, cardiac arrest presents differently in kids
67
How is propofol infusion syndrome treated?
Stop infusion Treat acidosis Support multi-system failure
68
How does propofol syndrome present in peds? Why so bad in peds?
- Anion gap metabolic acidosis - Bradyarrhythmia*** - Rhabdo - Liver dysfunction Leads to: - MODS - Hyperkalemia - AKI - Cardiac dysfunction - Death Kids can't metabolize fatty acids & they accumulate
69
Fospropofol (Lusedra)
Water soluble pro-drug of Propofol No need for lipid vehicle
70
Fospropofol vs Propofol?
Fospropofol: - slower onset - longer/stronger duration
71
Ketamine produces a _____ anesthesia, which is seen on ___.
Dissociative | EEG
72
With ketamine, patients are non____ and have a _____ _____.
``` communicative blank stare (cataleptic state) ```
73
Pro's and con's of Ketamine
Pro: Great pain control Cons: - No complete amnesia, needs a benzo - Emergence Delerium , reduced by benzo
74
Chemical structure of Ketamine
- Phencyclidine - partially water soluble - Has a racemic mixture (Ketanest)= more potent + less SE, but $$$
75
Ketamine Mechanism of Action | -receptors?
- NMDA receptor antagonist (blocks glutamate, excitatory neurotransmitter) - Weak action on GABA-A - May effect opioid, muscuranic, and monoaminergic receptors
76
How does ketamine produce it's analgesic effect?
Inhibits nitric oxide synthase
77
How does Ketamine stimulate Sympathetic system?
Inhibits reuptake of catecholamines
78
How does Ketamine produce Beta-2 agonism and respiratory relaxation?
Induces catecholamine release
79
Ketamine Pharmcokinetics - proteins? - distribution fast/slow? - hydro/lipophilic? - compartment model?
- Not bound to plasma proteins - Rapid distribution to tissues - Very Lipophilic, crosses BBB - 3 compartment model
80
Metabolism of Ketamine is in the _____. Demethylation of ketamine to ______, an ______ metabolite. This may produce _____ effects.
Liver norketamine active metabolite prolonged
81
Ketamine CNS effects: it's a cerebral vaso_____, therefore ______ cerebral BF & O2.
vasodilator | increases
82
In what population is ketamine NOT recommended?
Patient's with intracranial pathology
83
Ketamine CV effects: | It's a direct myocardial _____. These effects are usually masked by ______ of the sympathetic nervous system.
Depressant Stimulation
84
Ketamine produces significant, transient ______ in systemic BP, HR, and CO.
increases
85
Ketamine's respiratory system effects?
NO significant respiratory depression!!!!**** - response to CO2 is preserved - transient hypoventilation - short periods of apnea
86
Ketamine side effects?
- Emergence Reactions: 10-30% - Vivid Dreams, Out of Body Experience, Hallucinations - Can last hours - Nystagmus

Pharmacology (10 decks)

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