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

anesthetics Flashcards

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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
Benzos Prototype
Diazepam / Valium
26
2-3 x potency of diazepam
midazolam / versed
27
midazolam / versed effect time at site equilibratioin
0.9-5.6 minutes
28
rapid redistribution and short duration
midazolam / versed
29
midazolam / versed E1/2t
1 - 6.5 hours
30
GABA binds to \_\_\_\_\_\_\_\_
the 2 beta sites
31
benzos bind to the \_\_\_\_\_\_\_
1. gamma site 2. GABA-A
32
GABA receptor has distinct binding sites for
GABA, Barbituates, Benzos, ETOH
33
GABA receptors are found on the \_\_\_\_\_\_\_\_\_\_\_.
Post-synaptic memebranes in the CNS
34
Benzos have a built in ________ that prevents them form exceeding the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_of GABA inhabition.
1. Ceiling effect 2. physiologic maximum
35
Benzos effects and precautions in anesthesia
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
36
Benzos do not directly cause \_\_\_\_\_\_\_\_\_\_\_\_. They may do so if the pateint is ___________ or if their BP is elevated from \_\_\_\_\_\_\_\_\_
1. Hypotension 2. hypovolemic 3. anxiety
37
Location of pain modulating systmes
1. periaquaductal gray 2. hypothalamus 3. substantia gelatinosa
38
Opioids act at both _____ and _______ sites
Pre and Post synaptic
39
Binding at the Opioid receptor causes 1. \_\_\_\_\_\_\_\_\_\_ 2. \_\_\_\_\_\_\_\_\_\_ 3. \_\_\_\_\_\_\_\_\_\_ 4. \_\_\_\_\_\_\_\_\_\_
1. **decreased** neurotransmission 2. increased K conductance (**hyperpolarization**) 3. Ca++ channel **inactivation**- to a certain degree 4. **Immediate** decrease in neurotransmitter release
40
Opioid prototype
Morphine
41
Fentanyl Potency
100x morphine
42
Sufentanyl potency
1000x Morphine
43
Opioids ar cardiac stable and will not effect \_\_\_\_\_\_\_
SVR
44
Opioids and versed
Have a synergistic effect
45
Barbituate Prototype
Sodium Pentathol (Thiopentol)
46
Sodium Petnathol (thiopentol) mechanism of action
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)
47
Barbituates also depress the ___________ which causes sleep.
Reticular Activating System
48
Barbituates produce a functional inhibition of \_\_\_\_\_\_\_\_\_
the post synaptic neuron
49
Barbituate Uses
1. Sedation and Hypnosis 2. Induction agents 3. Cerebral Protection 4. Anti-seizure
50
How do Barbituates cause cerebral protection
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**
51
Why does thyopentol produce a hangover effect
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
52
Thiopentol cases depression of the _____________ center and decreases \_\_\_\_\_\_\_\_\_\_. This results in ___________ and decreased \_\_\_\_\_\_\_\_\_.
1. Medully Vasomotor Center 2. SNS outflow 3. peripheral vasodilation 4. preload
53
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.
1. SNS 2. Hypovolemic 3. ICP 4. significant decrease in BP 5. myocardial depression 6. Epinepherine
54
Thiopentol and Ventilation
1. Respiratroy depression with 2. Decreased RR and Decerease TV
55
1. causes **crystalization/gangrene/nerve** dammage 2. pain that radiates along **arterial distribution**
Intra-arterial injection of thiopentol
56
Treatment: 1. NS injection, lidocaine, papaverine, phenoxybenzamine 2. sympathectomy via brachial plexus block
Intra-arterial injection of thiopentol
57
Thiopentols effect is rapidly terminated because of \_\_\_\_\_\_\_\_\_\_\_\_\_
**Redistribution**, form brain (vessel rich) tissue to inactive sites (muscle, fat)
58
What is thiopentols E1/2 time?
11.6 hours
59
thiopentol especially effects ___________ because of the excess adipose tissue for the drug to redistribut into and then be removed from
Obese patients
60
What is the E1/2t for Propofol
0.5-1.5 hours
61
Phenobarbitol
Is the most potent CYP 450 inducer
62
Thopentol and metabolism
It is a POTENT CYP 450 inducer
63
Barbituates and metabolism
Hepatically and they **induce** the CYP 450 system
64
Barebituates produce a dose dependant depression in the _________ and \_\_\_\_\_\_\_\_\_centers. They cause decreased ventilatory response to __________ and \_\_\_\_\_\_\_\_\_\_\_. Thus cause \_\_\_\_\_\_\_\_
1. Medullary and pontine respiratory centers 2. Hypoxia and hypercapnea 3. Apnea
65
Because barbituates induce the enzyme induction systerm, they increase the metabolism of: 1. \_\_\_\_\_\_\_\_\_ 2. \_\_\_\_\_\_\_\_\_ 3. \_\_\_\_\_\_\_\_\_ 4. \_\_\_\_\_\_\_\_\_ 5. \_\_\_\_\_\_\_\_\_
1. oral anticoagulants 2. Vitamin K 3. Phenytoin 4. TCA's 5. Corticosteroids
66
Propofol drug classification
Non-barbituate intravenous anesthetic
67
Propofol is supplied as
1. 1% solution in **Egg, soy** and glycerol 2. **Anapahlactoid** reactions - avoid in Egg **yolk** and soy allergies
68
2 preservatives used in Propofol
1. EDTA - preffered 2. Sodium metabisulfite
69
Which preservative can cause bronchospasm in astmatics
Sodium metabasulfite
70
Preservatives in Propofol
1. Propofol **Inhibits** phagocytosis 2. preservatives likely kill off **S. Aures, E. coli and P. Aeruginosa** which popofol supports the growth of
71
Propofol Mechanism of Action
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
Propofols clearance ________ hepatic blood flow
Exceeds
73
Propofol Metabolism
conjugated in the liver to water souluable compounds
74
Propofol excretion
Renally - CRF doesn't affect clearance
75
the drug propofol is a \_\_\_\_\_\_\_\_\_\_\_, it is the preservative Na-metabasulfite that causes ____________ in astmatics
1. Bronchodialator 2. Bronchoconstriction
76
Even at at low doses propofol can serve as an\_\_\_\_\_\_\_\_\_\_ because it directly acts of \_\_\_\_\_\_\_\_\_\_\_\_\_\_.
1. Antiemetic 2. Chemo receptor trigger zone
77
Propofol produces dose dependant
sedation an hypnosis
78
Effects of Propofol
1. Sedation/hypnosis 2. Anesthesia 3. Amnesia 4. Antiemetic 5. Antiprueitic 6. Anticonvulsant 7. Attenuation of bronchoconstriction
79
Adverse effects of propofol
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
Cardiovascular effects of propofol
1. Vasodilation 1. Decreased SVR 2. Myocardial depression 1. Decreased SV 2. Decreased CO 3. Bradycardia????
81
Deaths with propofol and bradycardia
1.4 / 100,000
82
What if you give propofol and the patient is twitching
It is myoclonus
83
Barbituates and the placenta
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
Action potential at neuromuscular junction
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
Succinylcholine Pharmacologic Class
Depolarizing neuromuscular blockade
86
Vecuronium pharmacologic class
Non-depolarizing neuromuscular blockade
87
Succinylcholine Mechanism of Action
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
How long does it take for Succinylcholine to work
Immediate onset and lasts for 5 minutes
89
Why is succinylcholine depolarizing?
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
in contrast to ACh Succhs is not metabolized by
Acetylcholinesterases
91
Succhs can be uaed to treat a life threatening ___________ in smaller doses
Laryngospasm
92
Succinylcholine metabolism
1. Rapid **hydrolysis** by **pseudocholinesterase** - also called plasma cholinesterase 2. It is an **enzyme** in the liver and plasma
93
How is Succhinycholine block terminated?
By diffusion away from the neuromuscular junction - then taken up by plasma
94
Succhinylcholine adverse effects and precautions
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
Increased succeptibility to hyperkalemia with succhynlycholine
1. Burn patients 2. trauma 3. nerve dammage 4. neuromuscular disease 5. renal failure
96
Children and Succinylcholine
Usually given with atropine- because it can cause dysrhythmias
97
Vecuronium Mechanism of action
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
Vecuronium is an ________________ non-depolarizing muscle relaxant. Its onset is \_\_\_\_\_\_\_\_\_. And its duration of action is \_\_\_\_\_\_\_\_\_\_\_.
1. intermediate acting 2. 3-5 minutes 3. 20-35minutes
99
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
1. 70% 2. 80-90%
100
For intubation the dose of vecuronium is _______ than the maintinece dose. Why?
Larger - to facilitate quicker onset
101
Vecuronium will have a prolonges/unpredictable effects with.
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
Vecuronium and all non-depolarizers will have resistance with\_\_\_\_\_\_\_\_
Burn patients
103
In order to reverse a non-depolarizer what must be present? Why?
**Twitches**- if not present end plates are **fully blocked** and reversals may actually **prolong** the muscle relaxation
104
Why is recal the higest in the cardiac OR?
When patients are placed on bipass it adds a huge Volume of distribution and drug concentrations drop
105
Inhalational anesthetic prototype
Isoflurane
106
Isoflurane drug class
Inhalational anesthetic - Halogenated-methyl-ethyl-ether
107
Isoflurane mechanism of action
Not really know, works on GABA receptors
108
With anesthetic gasses less lipid soluable means \_\_\_\_\_\_\_\_\_\_
the drug has a quicker onset of action
109
In inhalational anesthetics what determines the onset, and duration
Lipid soluability - **less soluable** means the drug has a **quicker** onset
110
Isoflurane eliminaton
almost entirely by the **lungs**
111
Three inhaled agents commonly used in anesthetic practice
1. Isoflurane 2. Sevoflurane 3. Desflurane
112
Isoflurane has a ___________ and a __________ after it is dc'd than Sevoflurane and Desflurane
1. slower onset 2. longer duration of action
113
Usually for shorter/same day surgery, or anything that requires a quick wake up, these agents are used
1. Desflurane 2. Sevoflurane
114
Isofluarane Anesthetic Uses
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
Isoflurane and respiration
1. **Bronchodilator** 2. Respiratory **depression** 1. Increase **RR** 2. Decreased **TV** 3. oveall **decrease** in minute ventilation
116
Isoflurane and cardiovascular effects
1. **Dose dependant** cardiac depression 1. Decreased **CO** 2. Decreased **BP** 3. **Vasodilation**
117
1. Autosomal dominat mutation of the sarcoplamic reticulum calcium channel (ryanodine receptor)
Malignant Hyperthermia
118
Malignant hyperternia triggerd from exposure to succinylcholine or inhaled agents causes
Uncontrolled **calcium efflux** from the SR with **tetany** and **excessive heat generation**
119
What is used to treat malignant hyperthermia. What does it do?
Dantrolene- **blocks** the Ca++ realease from the SR
120
clinical signs of malignant hyperthermia
1. Muscle rigidity 2. Increased CO2 3. Increased temperature
121
MAC for inhaled agents
1. Mean Alveolar Concentration 1. of volitile anesthetic to which 50% of patients do not move to noxious stimuli 2. Describes potency
122
The lower the MAC the ________ the drug is
More potent
123
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 \_\_\_\_\_\_\_\_\_\_.
1. Starting point 2. higher than the MAC 3. lowe than the MAC 4. Cardiovascuar side effects
124
In monitored anesthesia care the patient 1. \_\_\_\_\_\_\_\_ 2. \_\_\_\_\_\_\_\_ 3. \_\_\_\_\_\_\_\_
1. Breathes on their own 2. remains respsive 3. may be in a light sleep
125
MAC of isoflurane
1.2%
126
Explain the flollowing gas mixture. Patient is on 100% oxygen and Isoflurane dialed to 1.2%
1. The patient is receiving 98.8% of oxygen monocules and 1.2% of Isoflurane molocules
127
Nitrous oxide MAC and its significance
1. **104%** 2. only inhaled agent that **by itself will not provide** 100% anesthesia
128
MAC is also comparable to the \_\_\_\_\_\_\_\_\_\_, so it essentially is the ____________ given to a patient
1. ED50 2. dose of anesthetic
129
0.5 MAC of Isuflurane is
0.6%
130
What is the MAC for desflurane
6%
131
0.5 MAC of desflurane
3%
132
133
Local anesthetics prototype
Lidocaine
134
Local anesthetic mechanism of action
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
Local anesthetic pharmacologic effect
Block **afferent** nerve transmission to produce **analgesia** and **anestheisa** without loss of conciousness
136
Blockade from local anesthetics includes: 1. \_\_\_\_\_\_\_\_\_ 2. \_\_\_\_\_\_\_\_\_ 3. \_\_\_\_\_\_\_\_\_
1. Autonomic Blockade 2. Somatic sensory blockade 3. Somatic motor blockade
137
2 classes of local anesthetics
1. One eyed **esters** and two eyed **amides** 2. Esters 3. Amides
138
Lidocaine pharmacologic class
1. **Amide** local anesthetics
139
typical local anesthetic structure
1. lipophilic **head** (aromatic ring) 2. intermediate **chain** 1. amide (NH) 2. ester (COO) 3. hydrophillic **tail** (tertiary amine)
140
Local anesthetic toxicitiey shows instability in the ___________ before __________ instability
1. brain 2. cardiac
141
Local anesthetic CNS toxicity
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
Tx for LA toxicity
Lipids, (Propofol- but iti isnt potent enough), benzos, pentathol, intubate- dont want to get to the seizure point
143
Bupivicaine is known for causing
1. Arrhythmias 1. AV heart block (AV node blocked heavily) 2. hypotension and arrest are VERY hard to overcome with Bupivicaine
144
Cocaine overdose
1. Manifests as massive sympathetic outflow - (Cocain structure very similar to NE) 2. Coronary vasospasm, MI 3. Dysrhythmias including V-fib
145
Cocain is very _______ acting
short
146
Bupivicain Pharmacologic class
Amide local anesthetic
147
Cocaine pharmacologic class
Ester local anesthetic
148
because of the structure being similar to NE, cocaine causes
euphoria

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

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