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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
Q

What are GABA-mimetic effects?

A

Barbiturates don’t need GABA with higher doses as opposed to Benzos

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26
Q

Barbiturates (reversibly/irreversibly?) bind to ____ ____.

A 
reversibly
plasma proteins (albumin)
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27
Q

What causes a higher unbound fraction of barbiturate, thus causing a greater clinical effect?

A

1) Decreased plasma protein concentrations
- Uremia
- Liver disease
- 3rd Trimester

2) Competition of other drugs for protein binding sites

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28
Q

What drugs compete with Barbiturates, thus increasing the unbound fraction of drug?

A

1) Aspirin
2) Naproxen
3) Indomethacin
4) Warfarin

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29
Q

Barbiturate absorption and distribution follow a __ compartment model

A

3

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30
Q

Barbs ____ metabolites are excreted in the ____.

A

inactive

urine

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31
Q

Barbiturate metabolism is in the ____ and is a ____ system ___.

A

Liver

CYP450 system inducer

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32
Q

CNS effect of barbiturate?
Analgesic?
Anticonvulsant?

A

Loss of consciousness in 10-30 seconds (level titratable)

NO analgesic effect

YES anticonvulsant-can abruptly stop seizures

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33
Q

Barbiturate CV effects?

A
  • Mass depression of vasomotor center
  • ↓BP from vasodilation
  • Compensatory ↑HR (may make ↓BP transient) *
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34
Q

Barbiturate Respiratory effects?

A
  • Depression
  • ↓response to CO2
  • Laryngospasm, bronchospasm!!!!
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35
Q

Barbiturates cause a dose dependent release of _____, which causes ____ and ____.

A

Histamine, which causes vasodilation and hypotension

36
Q

What happens with inadvertent intra-arterial injection of barbiturates?**

Treatment?

A
  • 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
Q

Absolute contraindication to barbituates

A
  • Hx allergic reaction

- Hx of Porphyria

38
Q

What do NMDA antagonists do?

A
  • Blocks receptor sites of NMDA to slow down propagation of action potential
  • Stops fight or flight hormones, therefore promote sedation
39
Q

Do barbs or benzos reduce CNS O2 and blood flow more?

A

Barbs

40
Q

Benzodiazepine Drugs

A
  • Librium
  • Diazepam
  • Serax
  • Lorazepam
  • Midazolam
41
Q

Benzodiazepine mechanism of action?

A
  • GABA-A agonist
  • Causes influx of Chloride ions ➞ hyperpolarizes neurons (less excitable)
  • Midazolam has greater potency & affinity for GABA-A (2-3x> diazepam)
42
Q

What are benzos used for?

A

Used often- broad scope of properties & low side effect profile

  • Anxiolytic
  • Sedation
  • Anticonvulsant
  • Muscle relaxation
  • Amnesia
43
Q

Why are benzos better over barbs?

A
  • Greater margin of safety against overdose***
  • Less abuse potential
  • Fewer/ less sig drug interactions
  • Do not induce hepatic microsomal enzymes
44
Q

What is special about the chemical structure of Midazolam?

A

Imidazole ring!

45
Q

Imidazole ring?

A

Versed Chemical Structure

  • In solution pH 4: OPEN
  • pH >4 (body): CLOSES & becomes lipophilic!!

Explains rapid onset 1-5min!

46
Q

Versed Pharmacokinetics

  • CNS onset?
  • relationship to proteins?
A
  • highly lipid soluble= enters CNS fast, but slow effect at site
  • highly protein bound
47
Q

Versed metabolism is in the ____ and is a CYP ___.

A

liver

CYP substrate

48
Q

Benzos are excreted in the ___.

A

urine

49
Q

Versed CNS effects

  • (CMRO2) Cerebral Metabolic Rate of O2 and CBF?
  • EEG?
  • ICP?
  • Neuroprotective?
  • Anti convulsant?
A
  • ↓CNS O2 & blood flow (but less than barbs)
  • Cannot produce isoelectric EEG
  • Cannot produce isoelectric EEG
  • Not neuroprotective
  • POTENT anticonvulsant properties**
50
Q

Versed CV effects

  • BP
  • SVR
  • CO
A
  • Hypotension d/t vasodilation ↓SVR (versed>diazepam)
  • CO no change
  • does not prevent sympathetic response to intubation (↑HR & BP)
51
Q

Versed Respiratory effects

A

(same as barbs, but lessened)

  • minimal, dose dependent decreased ventilation
  • ↓response to CO2
  • Synergistic and additive with opioids!!!** may cause apnea*
52
Q

Versed side effects

A
  • allergic rx rare
  • drowsiness>sedation
  • Sleep is not restorative*
  • Anterograde amnesia- alleviates anxiety**
53
Q

Withdrawal of Benzos and Barbs:

  • Duration?
  • CNS & CV effects?
A
  • can last weeks-months
  • CNS: anxiety, insomnia, seizures, coma, agitations, mania, psychosis, suicide
  • ↑HR, ↑BP, postural hypotension (deaths*)
54
Q

Benzo and Barb overdose:

  • Causes?
  • Reversal?
  • Tx?
A
  • Respiratory depression, hypotension, coma, confusion
  • Benzo ONLY reversal= flumanizel (caution in chronic users- immediate withdrawal can be = dangerous)
  • Tx: supportive therapy
55
Q

What is Flumazenil?

A
  • Reversal for benzos
  • Benzo antagonist- competitive
  • May require mult. doses
  • Versed has a longer 1/2 life than it
56
Q

Versed dosing

A

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
Q

Remimazolam

A
  • 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
Q

Propofol

  • Use
  • Chemical structure
A
  • Used for IV maintenance of general anesthesia

- insoluble & requires a lipid vehicle for emulsification**

59
Q

Drawbacks for propofol emulsification

A
  • Supports bacterial growth (6hr)
  • Allergies
    • soy & egg (depending on solution)
  • Asthmatic episodes & sulfite allergic rx in generic
60
Q

Propofol mechanism of action

A

Works on GABA-A receptors

61
Q 
Propofol pharmacokinetics:
Onset?
Duration?
Clearance?
Compartment model?
CYP?
A
  • 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
Q

Propofol CNS effects:

  • CNS O2 & Blood flow?
  • ICP?
  • IOP?
  • Neuroprotective?
  • Anti-epileptic?
A
  • ↓CNS O2 & blood flow
  • ↓ICP
  • ↓IOP
  • Neuroprotective during focal ischemia**
  • Anti-epileptic- yes (may cause twitching during induction- not seizure activity)
63
Q

Propofol CV effects:

  • BP
  • SVR
  • HR
A
  • ↓↓BP: vasodilation, ↓SVR, ↓preload

- Inhibition of baroreceptor reflex= ↓HR/BP

64
Q

Propofol Respiratory effects

A
  • potent respiratory depression
  • apnea after induction
  • ↓response to O2 & CO2
  • ↓↓upper airway reflexes
    (less spasm risk compared to benzos)
65
Q

Other propofol effects (benefits and SE)

A
  • 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
Q

What is propofol infusion syndrome (+adult presentation)?

A

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
Q

How is propofol infusion syndrome treated?

A

Stop infusion

Treat acidosis

Support multi-system failure

68
Q

How does propofol syndrome present in peds?

Why so bad in peds?

A
  • 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
Q

Fospropofol (Lusedra)

A

Water soluble pro-drug of Propofol

No need for lipid vehicle

70
Q

Fospropofol vs Propofol?

A

Fospropofol:

  • slower onset
  • longer/stronger duration
71
Q

Ketamine produces a _____ anesthesia, which is seen on ___.

A

Dissociative

EEG

72
Q

With ketamine, patients are non____ and have a _____ _____.

A 
communicative
blank stare (cataleptic state)
73
Q

Pro’s and con’s of Ketamine

A

Pro: Great pain control

Cons:

  • No complete amnesia, needs a benzo
  • Emergence Delerium , reduced by benzo
74
Q

Chemical structure of Ketamine

A
  • Phencyclidine
  • partially water soluble
  • Has a racemic mixture (Ketanest)= more potent + less SE, but $$$
75
Q

Ketamine Mechanism of Action

-receptors?

A
  • NMDA receptor antagonist (blocks glutamate, excitatory neurotransmitter)
  • Weak action on GABA-A
  • May effect opioid, muscuranic, and monoaminergic receptors
76
Q

How does ketamine produce it’s analgesic effect?

A

Inhibits nitric oxide synthase

77
Q

How does Ketamine stimulate Sympathetic system?

A

Inhibits reuptake of catecholamines

78
Q

How does Ketamine produce Beta-2 agonism and respiratory relaxation?

A

Induces catecholamine release

79
Q

Ketamine Pharmcokinetics

  • proteins?
  • distribution fast/slow?
  • hydro/lipophilic?
  • compartment model?
A
  • Not bound to plasma proteins
  • Rapid distribution to tissues
  • Very Lipophilic, crosses BBB
  • 3 compartment model
80
Q

Metabolism of Ketamine is in the _____. Demethylation of ketamine to ______, an ______ metabolite. This may produce _____ effects.

A

Liver
norketamine
active metabolite
prolonged

81
Q

Ketamine CNS effects: it’s a cerebral vaso_____, therefore ______ cerebral BF & O2.

A

vasodilator

increases

82
Q

In what population is ketamine NOT recommended?

A

Patient’s with intracranial pathology

83
Q

Ketamine CV effects:

It’s a direct myocardial _____. These effects are usually masked by ______ of the sympathetic nervous system.

A

Depressant

Stimulation

84
Q

Ketamine produces significant, transient ______ in systemic BP, HR, and CO.

A

increases

85
Q

Ketamine’s respiratory system effects?

A

NO significant respiratory depression!!!!**

  • response to CO2 is preserved
  • transient hypoventilation
  • short periods of apnea
86
Q

Ketamine side effects?

A
  • Emergence Reactions: 10-30%
  • Vivid Dreams, Out of Body Experience, Hallucinations
  • Can last hours
  • Nystagmus

Pharmacology (10 decks)

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