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!!!!! Pharm Spring 16 Exam 2 !!!!! > anesthetics > Flashcards

anesthetics Flashcards

1
Q

epidural, spinal, peropheral nerve block( Area and distributions of nerves)

A

Regional Anesthesia

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2
Q
  1. sedatives or other agents
  2. Patients responsive and breath without assistance
A

Monitored anesthesa

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3
Q

Mac and local/regional

A

Combination anesthesia car

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4
Q
  1. pt responds normally to verbal commands
  2. cognitive function and coordination may be impaired
  3. Ventilatory and CV functions unaffected
A

Minimal sedation (anxiolysis)

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5
Q
  1. Patient responed purposfully to verbal comands
    1. either alone or by light tactile stimulation
  2. Spontaneous ventilation is adequte
  3. CV function ususally maintained
A

Moderate sedation/analgesia (concious sedation)

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6
Q

Minimal sedation

A
  1. peripehral nerve blocks
  2. local/topical anesthesia
  3. less than 50% N20 in O2
  4. OR Single oral sedative/analgesic in doses appropriate fo UNSUPERVISED treatment of insomnia, anxiety or pain
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7
Q

Deep sedation provider requirements

A
  1. Provider should have no other responsibility
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8
Q

provider may assist with minor interruptable tasks once patients level of sedation -analgesia and vital signs have been stablized

A

moderate sedation provider requirements

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9
Q
  1. Not easily aroused
  2. respond purposfully to repeated.painful stimuli
  3. Ability to independant ventilatory function may be impaired
  4. Cardiovascular function os usually mantained
A

Deep sedation/Analagesia

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10
Q
  1. Not arousable even by painful stimuli
  2. Independent ventilatory function is impaired
  3. require assistance maintaining patent airway
  4. CV function may be impaired
  5. No sensory perception -Still has sensory input
A

General Anesthesia (Reversible)

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11
Q

Define general anesthesia

A
  1. generalized reversible CNS depression
    1. No sensory perception- has sensory input
    2. Loss of conciousness
    3. immobility
    4. some supression of autonomic reflexes
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12
Q

most general anesthetics require supplimentation of an _________ for __________ to occur

A
  1. opioid
  2. analgesia
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13
Q

In absense of an opoid the body will indicate the stress response via

A
  1. Increased HR, BP
  2. SNS activation
  3. Cortisol release
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14
Q

without intra-op opioids…..

A

post op pain controll is difficult to acheive

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15
Q

General anesthesia with ETT template

A
  1. Pre-op meds/sedation
  2. induction drug
  3. Neuromuscular blockade
  4. Inhalational drug
  5. Antiemetic
  6. Neuromuscular blockade reversal agent
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16
Q

Pre- meds/ sedation

A
  1. Anxiolytics- bezo
  2. antibiotic
  3. opioids
  4. prevent aspiration
  5. Preoxygenation
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17
Q

Induction drug

A
  1. IV or Inhalational
  2. IV = barbituate or non barbituate
  3. Inhalation = usually sevoflurane
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18
Q

Inhalation induction- usual drug and why

A
  1. Sevoflurane
  2. Isoflurane takes too long
  3. desflurane is to harsh on the airway
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19
Q

Neuromuscular blockade

A
  1. Facilitate intubation and optimize surgical conditions
  2. when the tube is in connect to circuit and turn on gas - induction drugs wear off in 3-5 minutes
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20
Q

Induction drugs

A

wear off in 3-5 minutes due to the distribution of the drug

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21
Q

Inhalational drug

A

for the maintinece of general anesthesia - may also be an IV drug

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22
Q

Opioids/local anesthetics

A
  1. minimize physiologic effects of pain
  2. promote comfort at emergence
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23
Q

Antiemetic

A

prevent nausea likely with inhalational agents and opioids

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24
Q

Reversal

A

reverse the paralyzong effects of neuromuscular blockade

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25
Q

Benzos Prototype

A

Diazepam / Valium

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26
Q

2-3 x potency of diazepam

A

midazolam / versed

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27
Q

midazolam / versed effect time at site equilibratioin

A

0.9-5.6 minutes

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28
Q

rapid redistribution and short duration

A

midazolam / versed

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29
Q

midazolam / versed E1/2t

A

1 - 6.5 hours

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30
Q

GABA binds to ________

A

the 2 beta sites

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31
Q

benzos bind to the _______

A
  1. gamma site
  2. GABA-A
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32
Q

GABA receptor has distinct binding sites for

A

GABA, Barbituates, Benzos, ETOH

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33
Q

GABA receptors are found on the ___________.

A

Post-synaptic memebranes in the CNS

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34
Q

Benzos have a built in ________ that prevents them form exceeding the _______________of GABA inhabition.

A
  1. Ceiling effect
  2. physiologic maximum
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35
Q

Benzos effects and precautions in anesthesia

A
  1. Dose dependant decrease in ventilation
  2. Hypoxemia and hypoventilation enhanced in presence of opioid
  3. Contraindicated in pregnancy
  4. Decreased SVR at induction doses
    1. very cardiac stable
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36
Q

Benzos do not directly cause ____________. They may do so if the pateint is ___________ or if their BP is elevated from _________

A
  1. Hypotension
  2. hypovolemic
  3. anxiety
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37
Q

Location of pain modulating systmes

A
  1. periaquaductal gray
  2. hypothalamus
  3. substantia gelatinosa
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38
Q

Opioids act at both _____ and _______ sites

A

Pre and Post synaptic

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39
Q

Binding at the Opioid receptor causes

  1. __________
  2. __________
  3. __________
  4. __________
A
  1. decreased neurotransmission
  2. increased K conductance (hyperpolarization)
  3. Ca++ channel inactivation- to a certain degree
  4. Immediate decrease in neurotransmitter release
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40
Q

Opioid prototype

A

Morphine

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41
Q

Fentanyl Potency

A

100x morphine

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42
Q

Sufentanyl potency

A

1000x Morphine

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43
Q

Opioids ar cardiac stable and will not effect _______

A

SVR

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44
Q

Opioids and versed

A

Have a synergistic effect

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45
Q

Barbituate Prototype

A

Sodium Pentathol (Thiopentol)

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46
Q

Sodium Petnathol (thiopentol) mechanism of action

A
  1. decreases rate at which GABA dissociates from the receptor (Enhances GABA)
    1. increases duration of CL- channel opening
  2. Mimics GABA at the receptor (direct activation of Cl- channels)
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47
Q

Barbituates also depress the ___________ which causes sleep.

A

Reticular Activating System

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48
Q

Barbituates produce a functional inhibition of _________

A

the post synaptic neuron

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49
Q

Barbituate Uses

A
  1. Sedation and Hypnosis
  2. Induction agents
  3. Cerebral Protection
  4. Anti-seizure
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50
Q

How do Barbituates cause cerebral protection

A
  1. By hyperoplarizing neurons with Cl- influx, the CMRO is decreased thereby producing less CO2 and causing cerebral vasoconstriction
  2. They do produce peripheral vasodilation
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51
Q

Why does thyopentol produce a hangover effect

A

It has a quick redistribution from the effect site and a long elimination half time, induction effect wears off quickly, but it still takes time for the body to eliminate the drug

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52
Q

Thiopentol cases depression of the _____________ center and decreases __________. This results in ___________ and decreased _________.

A
  1. Medully Vasomotor Center
  2. SNS outflow
  3. peripheral vasodilation
  4. preload
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53
Q

Thiopentol

If the _______is not intact or patient is _________ or if large doses are given to reduce _________. We will see ______________ and __________. Especially in the older population. Sometimes it is dosed with __________ to avoid this.

A
  1. SNS
  2. Hypovolemic
  3. ICP
  4. significant decrease in BP
  5. myocardial depression
  6. Epinepherine
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54
Q

Thiopentol and Ventilation

A
  1. Respiratroy depression with
  2. Decreased RR and Decerease TV
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55
Q
  1. causes crystalization/gangrene/nerve dammage
  2. pain that radiates along arterial distribution
A

Intra-arterial injection of thiopentol

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56
Q

Treatment:

  1. NS injection, lidocaine, papaverine, phenoxybenzamine
  2. sympathectomy via brachial plexus block
A

Intra-arterial injection of thiopentol

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57
Q

Thiopentols effect is rapidly terminated because of _____________

A

Redistribution, form brain (vessel rich) tissue to inactive sites (muscle, fat)

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58
Q

What is thiopentols E1/2 time?

A

11.6 hours

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59
Q

thiopentol especially effects ___________ because of the excess adipose tissue for the drug to redistribut into and then be removed from

A

Obese patients

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60
Q

What is the E1/2t for Propofol

A

0.5-1.5 hours

61
Q

Phenobarbitol

A

Is the most potent CYP 450 inducer

62
Q

Thopentol and metabolism

A

It is a POTENT CYP 450 inducer

63
Q

Barbituates and metabolism

A

Hepatically and they induce the CYP 450 system

64
Q

Barebituates produce a dose dependant depression in the _________ and _________centers. They cause decreased ventilatory response to __________ and ___________. Thus cause ________

A
  1. Medullary and pontine respiratory centers
  2. Hypoxia and hypercapnea
  3. Apnea
65
Q

Because barbituates induce the enzyme induction systerm, they increase the metabolism of:

  1. _________
  2. _________
  3. _________
  4. _________
  5. _________
A
  1. oral anticoagulants
  2. Vitamin K
  3. Phenytoin
  4. TCA’s
  5. Corticosteroids
66
Q

Propofol drug classification

A

Non-barbituate intravenous anesthetic

67
Q

Propofol is supplied as

A
  1. 1% solution in Egg, soy and glycerol
  2. Anapahlactoid reactions - avoid in Egg yolk and soy allergies
68
Q

2 preservatives used in Propofol

A
  1. EDTA - preffered
  2. Sodium metabisulfite
69
Q

Which preservative can cause bronchospasm in astmatics

A

Sodium metabasulfite

70
Q

Preservatives in Propofol

A
  1. Propofol Inhibits phagocytosis
  2. preservatives likely kill off S. Aures, E. coli and P. Aeruginosa which popofol supports the growth of
71
Q

Propofol Mechanism of Action

A
  1. Potentiates binding of GABA to GABA-A receptor at the B1 subunit
  2. Decreases the rate of disassociation of GABA from the receptor - increase Cl- influx (hyperpolarization and decreased neuronal excitability)
72
Q

Propofols clearance ________ hepatic blood flow

A

Exceeds

73
Q

Propofol Metabolism

A

conjugated in the liver to water souluable compounds

74
Q

Propofol excretion

A

Renally - CRF doesn’t affect clearance

75
Q

the drug propofol is a ___________, it is the preservative Na-metabasulfite that causes ____________ in astmatics

A
  1. Bronchodialator
  2. Bronchoconstriction
76
Q

Even at at low doses propofol can serve as an__________ because it directly acts of ______________.

A
  1. Antiemetic
  2. Chemo receptor trigger zone
77
Q

Propofol produces dose dependant

A

sedation an hypnosis

78
Q

Effects of Propofol

A
  1. Sedation/hypnosis
  2. Anesthesia
  3. Amnesia
  4. Antiemetic
  5. Antiprueitic
  6. Anticonvulsant
  7. Attenuation of bronchoconstriction
79
Q

Adverse effects of propofol

A
  1. Dose dependant respiratory depression
  2. dose dependant myocardial deprssion and vasodilatin
  3. Myoconus
  4. Lipidemia
  5. Pain on injection
  6. Infection and bronchospasm/preservatives
80
Q

Cardiovascular effects of propofol

A
  1. Vasodilation
    1. Decreased SVR
  2. Myocardial depression
    1. Decreased SV
    2. Decreased CO
    3. Bradycardia????
81
Q

Deaths with propofol and bradycardia

A

1.4 / 100,000

82
Q

What if you give propofol and the patient is twitching

A

It is myoclonus

83
Q

Barbituates and the placenta

A
  1. Barbituates readily cross the placenta
  2. levels much lower in fetal circulation than in maternal circulation
  3. Dose reduced in emergency C-section
84
Q

Action potential at neuromuscular junction

A

Pre synaptic

  1. Depolarization of nerve terminal
  2. VG Ca++ channel opens
  3. ACh vessicles spill into synaptic cleft

Post synaptically

  1. ACh binds to Alpha subunit of nicotinic receptors (2)
  2. Na++ opens and Na and Ca diffuses into cell, K+ diffuse out
  3. Motor end plate depolarizes
  4. Action potential causes muscle contraction
85
Q

Succinylcholine Pharmacologic Class

A

Depolarizing neuromuscular blockade

86
Q

Vecuronium pharmacologic class

A

Non-depolarizing neuromuscular blockade

87
Q

Succinylcholine Mechanism of Action

A
  1. Mimimics ACh and binds to alpha subunit of nicotinic receptors
  2. Has an immediate effect on the motor end plate, attaches to receptor longer than ACh, not allowing another action potential to take place
88
Q

How long does it take for Succinylcholine to work

A

Immediate onset and lasts for 5 minutes

89
Q

Why is succinylcholine depolarizing?

A
  1. When it binds to the nicotinic alpha subunit it causes a conformational change
  2. motor end plate depolarizes
  3. single contraction occurs
  4. further action potentials cannot be initiated until drug diffuses back into circulation
90
Q

in contrast to ACh Succhs is not metabolized by

A

Acetylcholinesterases

91
Q

Succhs can be uaed to treat a life threatening ___________ in smaller doses

A

Laryngospasm

92
Q

Succinylcholine metabolism

A
  1. Rapid hydrolysis by pseudocholinesterase - also called plasma cholinesterase
  2. It is an enzyme in the liver and plasma
93
Q

How is Succhinycholine block terminated?

A

By diffusion away from the neuromuscular junction - then taken up by plasma

94
Q

Succhinylcholine adverse effects and precautions

A
  1. Cardiac dysrhythmias
  2. Hyperkalemia
  3. Muscle Pains from fasciculations
  4. Increased ICP
  5. Increases Intraoccular pressure
  6. Triggers Malignant hyperthermia
  7. Pts with atypical acetylcholinesterases cannot metabolize
95
Q

Increased succeptibility to hyperkalemia with succhynlycholine

A
  1. Burn patients
  2. trauma
  3. nerve dammage
  4. neuromuscular disease
  5. renal failure
96
Q

Children and Succinylcholine

A

Usually given with atropine- because it can cause dysrhythmias

97
Q

Vecuronium Mechanism of action

A
  1. Competitive antagonism (reversible) at neuromuscular junction ACh receptors
  2. Occupes alpha subunit without producing conformational change - binds and doesnt produce action potential
  3. Blocks action potential
98
Q

Vecuronium is an ________________ non-depolarizing muscle relaxant. Its onset is _________. And its duration of action is ___________.

A
  1. intermediate acting
  2. 3-5 minutes
  3. 20-35minutes
99
Q
  1. Occupation of _________ of nicotinic ACh receptors can occur with little evidence of neuromuscular blockade.
  2. Neuromuscular transmission fails when _______ of the receptors are blocked
A
  1. 70%
  2. 80-90%
100
Q

For intubation the dose of vecuronium is _______ than the maintinece dose. Why?

A

Larger - to facilitate quicker onset

101
Q

Vecuronium will have a prolonges/unpredictable effects with.

A
  1. Liver and kidney disease
  2. Neuromuscular disease
  3. Hypothermia
  4. Electrolyte imblaances
  5. Antibiotics- aminoglycosides cause prolonged relaxation (PCN and cephalosporins have no effect)
102
Q

Vecuronium and all non-depolarizers will have resistance with________

A

Burn patients

103
Q

In order to reverse a non-depolarizer what must be present? Why?

A

Twitches- if not present end plates are fully blocked and reversals may actually prolong the muscle relaxation

104
Q

Why is recal the higest in the cardiac OR?

A

When patients are placed on bipass it adds a huge Volume of distribution and drug concentrations drop

105
Q

Inhalational anesthetic prototype

A

Isoflurane

106
Q

Isoflurane drug class

A

Inhalational anesthetic - Halogenated-methyl-ethyl-ether

107
Q

Isoflurane mechanism of action

A

Not really know, works on GABA receptors

108
Q

With anesthetic gasses less lipid soluable means __________

A

the drug has a quicker onset of action

109
Q

In inhalational anesthetics what determines the onset, and duration

A

Lipid soluability - less soluable means the drug has a quicker onset

110
Q

Isoflurane eliminaton

A

almost entirely by the lungs

111
Q

Three inhaled agents commonly used in anesthetic practice

A
  1. Isoflurane
  2. Sevoflurane
  3. Desflurane
112
Q

Isoflurane has a ___________ and a __________ after it is dc’d than Sevoflurane and Desflurane

A
  1. slower onset
  2. longer duration of action
113
Q

Usually for shorter/same day surgery, or anything that requires a quick wake up, these agents are used

A
  1. Desflurane
  2. Sevoflurane
114
Q

Isofluarane Anesthetic Uses

A
  1. sedation and hypnonsis
  2. muscle relaxation
  3. Maintinece of general anesthesia - dont use for Monitored anesthesia care
  4. Induction (usually sevoflurane only)
  5. Bronchodilatior
115
Q

Isoflurane and respiration

A
  1. Bronchodilator
  2. Respiratory depression
    1. Increase RR
    2. Decreased TV
    3. oveall decrease in minute ventilation
116
Q

Isoflurane and cardiovascular effects

A
  1. Dose dependant cardiac depression
    1. Decreased CO
    2. Decreased BP
    3. Vasodilation
117
Q
  1. Autosomal dominat mutation of the sarcoplamic reticulum calcium channel (ryanodine receptor)
A

Malignant Hyperthermia

118
Q

Malignant hyperternia triggerd from exposure to succinylcholine or inhaled agents causes

A

Uncontrolled calcium efflux from the SR with tetany and excessive heat generation

119
Q

What is used to treat malignant hyperthermia. What does it do?

A

Dantrolene- blocks the Ca++ realease from the SR

120
Q

clinical signs of malignant hyperthermia

A
  1. Muscle rigidity
  2. Increased CO2
  3. Increased temperature
121
Q

MAC for inhaled agents

A
  1. Mean Alveolar Concentration
    1. of volitile anesthetic to which 50% of patients do not move to noxious stimuli
  2. Describes potency
122
Q

The lower the MAC the ________ the drug is

A

More potent

123
Q

We generally use MAC as a ____________. Generaly the youger the patient will need gas concentrations ___________ and the elderly will need gas concentrations __________. If gasses are dialed too high for the patient we may see __________.

A
  1. Starting point
  2. higher than the MAC
  3. lowe than the MAC
  4. Cardiovascuar side effects
124
Q

In monitored anesthesia care the patient

  1. ________
  2. ________
  3. ________
A
  1. Breathes on their own
  2. remains respsive
  3. may be in a light sleep
125
Q

MAC of isoflurane

A

1.2%

126
Q

Explain the flollowing gas mixture.

Patient is on 100% oxygen and Isoflurane dialed to 1.2%

A
  1. The patient is receiving 98.8% of oxygen monocules and 1.2% of Isoflurane molocules
127
Q

Nitrous oxide MAC and its significance

A
  1. 104%
  2. only inhaled agent that by itself will not provide 100% anesthesia
128
Q

MAC is also comparable to the __________, so it essentially is the ____________ given to a patient

A
  1. ED50
  2. dose of anesthetic
129
Q

0.5 MAC of Isuflurane is

A

0.6%

130
Q

What is the MAC for desflurane

A

6%

131
Q

0.5 MAC of desflurane

A

3%

132
Q
A
133
Q

Local anesthetics prototype

A

Lidocaine

134
Q

Local anesthetic mechanism of action

A
  1. block impulse conduction during depolarization of action potential by inhibition of the influx of Na+ ions
  2. Block only occurs when Na channels are in the inactive closed state - it cannot effect activated open channels
135
Q

Local anesthetic pharmacologic effect

A

Block afferent nerve transmission to produce analgesia and anestheisa without loss of conciousness

136
Q

Blockade from local anesthetics includes:

  1. _________
  2. _________
  3. _________
A
  1. Autonomic Blockade
  2. Somatic sensory blockade
  3. Somatic motor blockade
137
Q

2 classes of local anesthetics

A
  1. One eyed esters and two eyed amides
  2. Esters
  3. Amides
138
Q

Lidocaine pharmacologic class

A
  1. Amide local anesthetics
139
Q

typical local anesthetic structure

A
  1. lipophilic head (aromatic ring)
  2. intermediate chain
    1. amide (NH)
    2. ester (COO)
  3. hydrophillic tail (tertiary amine)
140
Q

Local anesthetic toxicitiey shows instability in the ___________ before __________ instability

A
  1. brain
  2. cardiac
141
Q

Local anesthetic CNS toxicity

A
  1. Circumoral/tongue numbness
  2. metalic taste
  3. tinnitus
  4. vision changes
  5. diziness
  6. slurred speech
  7. restlessness
  8. seizure
  9. CNS depression
  10. apnea
  11. hypotension (decreased SVR and CO)
  12. cardiovascualr collapse
142
Q

Tx for LA toxicity

A

Lipids, (Propofol- but iti isnt potent enough), benzos, pentathol, intubate- dont want to get to the seizure point

143
Q

Bupivicaine is known for causing

A
  1. Arrhythmias
    1. AV heart block (AV node blocked heavily)
    2. hypotension and arrest are VERY hard to overcome with Bupivicaine
144
Q

Cocaine overdose

A
  1. Manifests as massive sympathetic outflow - (Cocain structure very similar to NE)
  2. Coronary vasospasm, MI
  3. Dysrhythmias including V-fib
145
Q

Cocain is very _______ acting

A

short

146
Q

Bupivicain Pharmacologic class

A

Amide local anesthetic

147
Q

Cocaine pharmacologic class

A

Ester local anesthetic

148
Q

because of the structure being similar to NE, cocaine causes

A

euphoria

!!!!! Pharm Spring 16 Exam 2 !!!!! (11 decks)

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