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Pharmacology > Induction Agents - quiz 2 > Flashcards

Induction Agents - quiz 2 Flashcards

1
Q

Where is site of action of medications?

A

receptor site on the neurons

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2
Q

Is GABA inhibitory or excitatory?

A

inhibitory

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3
Q

Is glutamate inhibitory or excitatory?

A

excitatory

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4
Q

GABA has _____ subunits and _____ subclasses

A 
5 subunits 
3 subclasses ( alpha, beta, gamma)
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5
Q

Everything besides _______ needs GABA to bind

A

Barbituates

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6
Q

GABA is a product of?

A

Glutamate

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7
Q

When GABA binds to its receptor, what electrolyte is moving though?

A

Chloride

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8
Q

NMDA is inhibitory or excitatory?

A

excitatory

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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

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10
Q

How does Alpha 2 work?

A

with the negative feedback loop and norepinephrine

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11
Q

What is a baroreceptor?

A

pick up pressure changes - send information to CNS and releases natural catecholamine’s

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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

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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

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14
Q

Duration of effect for boluses is how long?

A

5-9 minutes

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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
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16
Q

IV induction agents are all what?

A

Lipophilic

aka non-ionized/lipophilic/hydrophobic

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17
Q

The first place IV meds will go is?

A

highly perfused organs (brain, heart, lung)

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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

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19
Q

What is
Compartment 1
Compartment 2
Compartment 3

A

1 - systemic circulation
2 - highly vascular organs
3 - fatty tissues

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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.

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21
Q

2 compartment model assumes that

A

after injection, medication distributes to highly vascular organs than to entire body

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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

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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

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24
Q

Barbiturates where created when?

A

In the 30’s - oldest meds we have

over 2000 different barbiturate agents

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25
Q

What are the 3 clinical effects we get from barbituates?

A

Sedative, hypnotic, anticonvulsant

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26
Q

Barbituric acid lacks what?

A

CNS activity.

Hypnotic, sedative and anticonvulsant effects occur through substitutions on the N1, C2, & C5 sites.

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27
Q

thiopental has pain with injection due to?

A

Alkaline (pH >10

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28
Q

Why wouldn’t Italy ship thiopental to the US

A

we were using it for lethal injection

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29
Q

What is the difference between methohexital and thiopental?

A

methohexital is ULTRA short acting (otherwise they are the same)

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30
Q

What is the MOA of barbiturates?

A

Post-synaptic enhancement of GABA mediated inhibitory neurotransmitters.

May also have GABA-mimetic effects.

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31
Q

Why can barbituates have high rates of overdose?

A

(GABA mimetic effects) they can activate GABA receptor on own with out help of normal GABA molecule binder.

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32
Q

how is barbituates bound?

A

protein bound

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33
Q

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

A

increased barbiturate levels and potential for toxicity

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34
Q

Barbiturates follow what type of absorption and distribution?

A

3 compartment model

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35
Q

Barbiturates are broken down into what for excretion?

A

Inactive metabolites

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36
Q

Barbiturates cause what during post anesthesia?

A

significant post anesthesia drowsiness

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37
Q

Does barbiturates have any analgesic properties?

A

no

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38
Q

Barbiturates has a decreased effect on what CNS properties?

A
  • Decrease in CMRO2
  • Decrease in CBF
  • Decrease in ICP and IOP
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39
Q

Anesthetic doses or barbiturates have anticonvulsant properties and can do what?

A

Abruptly stop seizures

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40
Q

Cardiovascular effects of barbiturates include

A

decrease in BP d/t peripheral vasodilation and DECREASED CO.

Rapid injection and large induction doses will have more profound effect in BP

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41
Q

Respiratory effects of barbiturates include

A
  • Resp depression
  • Decreased minute ventilation
  • Laryngospasm, bronchospasm – give lidocaine to blunt spams response
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42
Q

Barbiturates cause a decrease in chemoreceptors which cause what?

A

Decrease in stimulation by CO2 to breathe and Decrease in ventilatory response to hypercapnia and hypoxia.

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43
Q

Barbituates and with morphine cause a release of what?

A

Histamine - When you have histamine releases from certain medications it can compound effects

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44
Q

Inadvertent intra-arterial injection of barbiturate can cause

A

Immediate vasospasm and severe vasoconstriction

treatment is: Dilution of drug by injection of normal saline through failed access site.

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45
Q

Treatment of vasospasm d/t intra-arterial injection of a bariturate

A

papaverine 40-80mcg.

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46
Q

Absolute contraindications for administration of barbiturates

A

allergic reactions and history of porphyria

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47
Q

What happens if you give a barbiturate to someone with porphyria?

A

Excitatory seizures, tachycardia and HTN, abd pain, N/V

opposite effects of what you would normally see with barbiturates

48
Q

How old are Benzos

A

Approx 45 years

49
Q

Why are Benzos used in many clinical situation?

A

Broad scope of properties and low side effect profile

50
Q

What properties do Benzos provide?

A

Anxiolytic, sedation, anticonvulsant, muscle relation, amnesia

51
Q

What is different about Benzos and barbituates in regards to safety?

A

Greater margin of safety against overdose

52
Q

Important part of chemical structure with benzos

A

Benzodiazepine ring

imidazole ring – ring stays closed making it even more lipophilic at physiologic pH

53
Q

Do Benzos need a lipid vehicle?

A

no

54
Q

In physiologic pH, ______ the diazepine ring closes and midazolam becomes _______.

A

(>4)

lipophilic

55
Q

Versed onset, peak and duration

A

Onset 1-5 min
Peak 30 minutes
Duration 2 hours

56
Q

Versed is ______ _______ soluble and _______ ________ bound

A

lipid soluble

protein bound

57
Q

Versed is a CYP _______

A

Substrate

58
Q

How is versed excreted?

A

Via urinary excretion

59
Q

Despite rapid passage into the brain, midazolam has a

A

slower effect site equilibrium

60
Q

What is the MOA of versed

A

Activation of GABA(A) receptor complex and enhancement of GABA mediated chloride currents.

61
Q

Why do we use versed more with induction than other benzo

A

high reliability, predictable, and effectiveness on GABA A receptors.

62
Q

GABA receptors responsive to benzodiazepines occur almost exclusively on

A

post-synaptic nerve endings in the CNS

63
Q

Benzos, compared to barbituates, decrease

A

CMRO2 and CBF

64
Q

Benzos ____________ produces and isoelectric line

A

CANNOT

65
Q

Benzos produce what in regards to ICP

A

Little to no change in ICP

66
Q

Benzos have __________ anticonvulsant properties

A

Potent

67
Q

Versed causes paradoxical excitement in <1 % of pt. What is paradoxical excitement

A

person not going to sleep – instead greatly agitated

68
Q

Benzos cause a _______ ________ decerase in systemic ___________

A

Dose Dependent

blood pressure

69
Q

Post induction hypotension is greater after ___________ then ___________

A

midazolam than diazepam.

70
Q

Is cardiac output changed with Bezos?

A

NO

71
Q

What type of amnesia can versed cause?

A

Anterograde amnesia

72
Q

What happens when you use benzos for sleep aids?

A

Sleep is not restorative, not hitting REM cycle

73
Q

How long can withdrawal from Benzos last?

A

Weeks to months

be careful with giving flumazonal - you can force pt into withdrawal if they have been taking them long term

74
Q

Benzos and barbituates cause significant hyperpolarization, which causes

A

a global reduction in output in CNS

75
Q

Benzo and barb over dose can cause Respiratory depression, hypotension, coma, confusion. What is your treatment?

A

Mostly use supportive therapy

76
Q

What is flumazonal?

A

Benzo antagonist- competitive

77
Q

Why does flumazonal usually need redosed?

A

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
Q

What is Remimazolam?

A

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
Q

What is the most frequently administered drug for induction of anesthesia?

A

Propofol

good consistent, predictable sedation

80
Q

Propofol is insoluble, therefor it needs what for emulsification?

A

lipid vehicle

81
Q

What allergy would prevent you from using propofol?

A

egg allergy (lipid vehicle has egg protein)

82
Q

Why does propofol need changed every 6 hours?

A

rate of bacterial growth after 6 hours exponentially increases!!

(increases risk of pts getting infections)

83
Q

Addition of preservatives in propfol inhibits bacterial growth for up to

A

12 hours

84
Q

What is in the Baxter and Pfizer brands of propofol that is not present in AstraZeneca brands that can lead to an asthma attack?

A

sulfite

85
Q

Propofol MOA

A

relatively selective modulator of GABA(A) receptors

86
Q

Onset, peak and duration of Propofol

A

Onset 30 seconds
Peak
Duration 3-10 minutes

87
Q

In comparing barbs and benzos to propofol, why does propofol have less of a “hangover” effect?

A

hepatic clearances than just liver (also lungs and biliary system)

88
Q

Propofol is a CPY _______ and _________

A

Substrate and inhibitor

89
Q

Propofol is ________ during times of focal ischemia

A

Neuroprotective

90
Q

What might you observe during induction with propofol?

A

May observe twitching or spontaneous movement (this is NOT seizure activity)

91
Q

Propofol and Benzos both has a profound decrease in systemic blood pressure due to

A

massive vasodilation

92
Q

Propofol has a dramatic inhibition of what reflex?

A

Baroreceptor and chemoreceptors

Profound bradycardia and hypotension in healthy adults
(Decrease ventilatory response to hypoxia and hypercapnia)

93
Q

Propofol causes less laryngospasms than what other med?

A

Barbituates

94
Q

Is propofol painful on injection?

A

YES - give 1% lidocaine prior

95
Q

What is a major benefit of propofol in post?

A

Decreased PONV!

96
Q

Explain propofol infusion syndrome

A
  • lactic acidosis
  • Kidney failure, rhabdomyolysis, cardiac arrest
  • UNEXPLAINED tachycardia (1st thing you will see)
  • Hypertrigyceridemia
97
Q

What is different about Fospropofol in its make up?

A

Does not require a lipid vehicle, (water soluble prodrug)

98
Q

If Fospropofol can have less “bad” effects on the body, why is it not used more?

A

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
Q

Ketamine causes what type of anesthesia?

A

dissociative

100
Q

Katamine causes a dissociation between what systems?

A

between thalamocortical and limbic system

101
Q

What type of state will the pt be in when they have been given ketamine?

A

cataleptic state with eyes open and slow nystagmic gaze

noncomunicative

102
Q

Ketamine can cause delirium, but how do you have to treat it?

A

Don’t treat delirium when its happening, you CAN pretreat for it prophylactically

103
Q

Does ketamine help with pain?

A

YES, good analgesic effect (reduces opiate use up to 50%)

104
Q

In regard to chemical structure, ketamine has a racemic mixture. What does this mean?

A

Ketamine is a mix of S and R antiomeres.

S more potent than R, AND less psych side effects.

105
Q

what is different with Ketamine in regards to protein binding than barbituates, Benzos and Propofol?

A

Ketamine is NOT significantly bound to protein

low albumin levels - burn pts, kidney failure, malnutrition - leads to toxic levels of ketamine

106
Q

In metabolism of Ketamine, what is different about its metabolite in comparison to barbs, benzos and propofol?

A

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
Q

Ketamine onset, peak and duration

A

Onset - 30-60 seconds
Peak 1 min
Duration 8-10 minutes (up to 25 min if IM)

108
Q

How do you administer ketamine?

A

slowly, over 60 seconds

109
Q

What is the MOA for ketamine?

A

NMDA receptor antagonist

Exerts weak action at GABA(A) receptor.

110
Q

Ketamine is a cerebral vasodilator, which increases?

A

CBF and CMRO2

NOT recommended for its with intracranial pathology

111
Q

How does ketamine cause sedation?

A

by blocking excitatory effects

112
Q

What kind of movement may you see on injection of ketamine?

A

Myoclonic movements

113
Q

Katamine has Centrally mediated sympathetic stimulation which causes an increase in

A

BP, HR and CO

increased CO gives way to increased CVP

114
Q

What is the effect of ketamine on the respiratory system?

A

No significant respiratory depression

115
Q

What are some emergence reactions from ketamine?

A

Vivid dreams, extracorporeal experiences, hallucinations

Pharmacology (8 decks)

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