Cumulative Final (Exam 2) Flashcards

(108 cards)

1
Q

What four groups will intravenous medications be distributed to?

What is the CO% of each group?

A

Vessel rich group (75%)
Muscle group (18%)
Fat (5%)
Vessel poor group (2%)

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2
Q

What are the 5 components of General Anesthesia?

A

Hypnosis
Analgesia
Muscle Relaxation
Sympatholysis (hemodynamic stability)
Amnesia

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3
Q

What are the 4 stages of General Anesthesia?

A

Stage 1: Analgesia
Stage 2: Delirium
Stage 3: Surgical Anesthesia
Stage 4: Medullary Paralysis

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4
Q

What are the 3 lower airway reflexes?

A

Coughing
Gagging
Swallowing

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5
Q

What is the upper airway reflex?

A

Sneezing

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6
Q

Which stage is prolonged during emergence?
Why?

A

Stage 2
Anesthetics are redistributed back into the blood from the tissues

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7
Q

What is the MOA of Barbituates?

A

Potentiates GABA-A channel activity; directly mimics GABA

Acts on glutamate, adenosine, and neuronal nicotinic acetylcholine receptors

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8
Q

Barbiturates are a cerebral _____________.

What will be the effect on CBF?
What will be the effect on CMRO2?

A

Cerebral vasoconstrictor

CBF decreases
CMRO2 decreases by 55%

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9
Q

When the barbiturate is non-ionized it will be ____ soluble, favoring ____.

A

more lipid soluble and acidosis

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10
Q

When the barbiturate is ionized, it will be ____ soluble, favoring ____ .

A

less lipid soluble and alkalosis

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11
Q

What are examples of oxybarbiturates?

A

Methohexital
Phenobarbital
Pentobarbital

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12
Q

What are examples of thiobarbiturates?

A

Thiopental
Thiamylal

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13
Q

Describes the distribution of a given agent at equilibrium between two substances at the same temperature, pressure, and volume?

A

Partition coefficient

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14
Q

What does a higher blood-gas coefficient correlate with?

A

Higher solubility of anesthetic in the blood and thus slowing the rate of induction. The blood can be considered a pharmacologically inactive reservoir.

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15
Q

What are the excitatory phenomenon with methohexital?

A

Myoclonus and Hiccups

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16
Q

Methohexital is used to induce seizures in patients undergoing _____ .

A

Temporal lobe resection (lower seizure threshold, easier for seizures to occur)

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17
Q

Barbiturates will cause ____ release, potentially leading to anaphylaxis if previously exposed.

A

Histamine

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18
Q

What is the side effect of barbiturates through intra-arterial injection?

Treatment?

A
  • Immediate intense vasoconstriction and pain.
  • Obscures distal arterial pulses → blanching, followed by cyanosis.
  • Gangrene and permanent nerve damage.

Treatment: Vasodilators - (lidocaine and papaverine), prevent vasospasm and sustain adequate blood flow

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19
Q

Propofol is a ____ agonist.

A

Gamma Aminobutyric Acid (GABA) agonist

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20
Q

Propofol is packaged with a mixture of what 3 ingredients?

A

Soybean oil
Glycerol
Purified egg phosphatide (lecithin)

Lecithin is part of the EGG YOLK - allergies

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21
Q

What are the commercial preparations for propofol?

A

Ampofol (low lipid emulsions with no preservatives, higher incidence of pain on injection)

Aquavan (prodrug that eliminates pain on injection, byproduct will produce perineal buring, larger Vd, slower onset, high potency)

Nonlipid with Cyclodextrins (studies show significantly more pain on injection)

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22
Q

Immobility from propofol is not caused by drug-induced ____ .

A

Spinal cord depression

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23
Q

What metabolizes propofol?

What does it metabolize to?

Where is propofol excreted?

A

Hepatic enzyme cytochrome P450

Water soluble glucuronic acid metabolites

Excreted by the kidneys

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24
Q

Propofol awakening times with cirrhosis of the liver?

A

No major difference due to rapid extrahepatic clearance

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25
The anti-emetic effects of propofol are more effective than _______. What is propofol's MOA for its anti-emetic effect?
Zofran Propofol depresses the subcortical pathways and has a direct depressant effect on the vomiting center.
26
Other benefits of propofol include: Propofol as a bronchodilator ________ at low doses Potent ________ Does not trigger _______
Other benefits of propofol include: Propofol as a bronchodilator **Analgesia** at low doses Potent **antioxidant** Does not trigger **MH**
27
What is the effect on HR with propofol?
Bradycardia d/t decreased SNS response, may depress baroreceptor reflexes preventing compensatory tachycardia. Profound bradycardia and asystole happens even in healthy adults.
28
What is the cause of PRIS? What will this cause in children? Signs/Sx? Reversible?
High dose infusion, greater than 75 μg/kg/min for 24 hours. Cause severe, refractory, and fatal bradycardia in children Symptoms: **Lactic acidosis, bradycardia, rhabdomyolysis**, green urine Reversible in the early stages
29
What is the treatment for someone with PRIS in cardiogenic shock?
Treatment: Extracorporeal membrane oxygenation (ECMO)
30
How does an increased ratio of fat to body weight affect ideal body weight dosing? Why is this?
It decreases the blood volume (mL/kg) Adipose tissue has decreased blood supply
31
Due to etomidate containing 35% ____ as a carrier agent, there will be pain at the injection site and venous irritation.
propylene glycol ## Footnote Textbook says now formulated with lipids so it doesn't burn
32
Etomidate is the only induction drug with direct systemic absorption in the oral mucosa that bypasses ___________.
Hepatic Metabolism *The percentage of the active drug does not decrease if given PO due to bypassing hepatic metabolism.*
33
What is Etomidate's MOA?
Directly and Indirectly opens Cl- channels of GABAA receptors
34
How is Etomidate metabolized?
Hydrolysis by hepatic microsomal enzymes and plasma esterases.
35
Etomidate is best suited for what type of patients for induction?
Unstable Cardiovascular patients, especially the ones with little or no cardiac reserves.
36
What is the primary side effect seen with etomidate? How can this be mitigated? What patients would we use caution with because of this?
* Involuntary myclonic movements * Pre-administering opiods (fentanyl 1-2 mcg/kg IV) or benzos * History of seizures
37
Rank these drugs from highest incidence of myoclonus to least: Propofol, thiopental, methohexital, and etomidate
Etomidate (50-80%) Thiopental (17%) Methohexital (13%) Propofol (6 %)
38
What does this graph tell you?
Etomidate is associated with a decrease in the plasma concentration of cortisol.
39
Like most of our barbiturates (thiopental), etomidate is a potent direct cerebral _________. What does this do to ICP?
Vasoconstrictor Decrease ICP
40
Ketamine is a derivative of _______. Why is this drug used for induction?
Phencyclidine (PCP) *Angel Dust* Ketamine is used for its amnestic and intense analgesic properties.
41
What advantages does ketamine have over propofol and etomidate?
* No pain on injection. * Profound analgesia at subanesthetic doses.
42
MOA of Ketamine (3)
1. Binds noncompetitively to **N-methyl-D-aspartate (NMDA)** receptor. This will inhibit the activation of the NMDA receptors by glutamate and decrease the presynaptic release of glutamate. 2. Ketamine will also bind to opioid receptors (mu, delta, kappa) and weak bind to sigma receptors. *analgesic effects* 3. Ketamine will have weak actions at GABA-A receptors
43
Ketamine can induce ____ . Therefore, the maintenance of pharyngeal and laryngeal reflexes (coughing/laryngospasm) is crucial. What can be given to mitigate this?
salivary secretions Glycopyrrolate
44
What are the components of the coronary artery disease cocktail?
Diazepam 0.5mg/kg IV Ketamine 0.5mg/kg IV Continuous Ketamine infusion 15-30 mcg/kg/min IV
45
CNS side effects of ketamine: Potent cerebral ___________. Can increase CBF by ____%
CNS side effects of ketamine: Potent cerebral **vasodilator**. Can increase CBF by **60%**
46
CV effects of ketamine?
Resembles SNS stimulation. There will be an increase in SBP, PAP, HR, CO, and MRO2. Increase plasma Epi and NE levels.
47
How does ketamine cause emergence delirium? How do you mitigate emergence delirium?
Depression of the inferior colliculus and medial geniculate nucleus Mitigate by giving BZD 5 minutes prior to ketamine administration.
48
What is the sensory-discriminitive portion of pain?
* The perception of pain by the brain; ascending pathway * spinothalamic/trigemino-thalamic tracts → somatosensory cortex
49
What is the motivational-affective portion of pain?
* The *responses* to painful stimuli * Attention/arousal * Somatic/autonomic reflexes * Endocrine response * Emotional response
50
Term for increased pain sensations to normally painful stimuli
Hyperalgesia
51
Term for perception of pain sensations in response to *normally* non-painful stimuli
Allodynia
52
List the steps in the pain perception pathway
1. **Transduction** - of pain via peripheral nociceptors 2. **Transmission** - of pain via nerves 3. **Modulation** - (inhibition/exitation) of pain at the dorsal root ganglion and dorsal horn 4. **Perception** - of pain via ascending spinothalamic tract at the somatosensory cortex
53
This brain strutctire acts at the central relay station for incoming pain signals
Thalamus
54
Unmyelinated C-fibers transmit what signals?
burning and pressure
55
The increased responsiveness of peripheral neurons responsible for pain transmission to heat, cold, mechanical or chemical stimulation is called ____?
Sensitization
56
What population has a decreasd pain threshold and exaggerated pain responses?
Neonates Pain perception at 23 weeks
57
These laminae synapse with afferent C fibers? Which one does opioids work on?
Lamina I (lamina marginalis) Lamina II (substantia gelatinosa) - *opioids work here*
58
Briefly describe the gate control theory of pain?
There is a neurologic "gate" in the doral horn that can be opened or closed. **Opened** = pain projected to supraspinal regions **Closed** = pain transmission to the brain is inhibited by simultaneous inhibitory impulses
59
What fiber type can cause the pain gate to close? How?
Aβ fibers (pressure/touch) - they are very large and myelinated; overriding the signals from slower nerve impulses (A𝜹 and C) An example would be rubbing your elbow after hitting it on something- the sharp, intense pain is overridden by the pressure sensations
60
What two areas in the brainstem depress or integrate pain in the spinal dorsal horn?
* Periaqueductal gray * Rostral ventral medulla
61
This area of the brain percieves the location and intensity of pain transmissions?
Forebrain SI and SII - This area is synonomous with the somatosensory cortex
62
These 2 areas on the brain are involved in the emotional and motivational aspects of pain?
* Anterior cingulate cortex (ACC) * Insular cortex (IC)
63
What are the neurotransmitters used in the descending inhibitory tract?
- Endorphins - Enkephalins - Serotonin
64
What 3 drugs are the phenanthrenes?
* Morphine - Codeine - Thebaine
65
What 2 opioids are benzylisoquinolines?
- Papaverine - Noscapine
66
Where are opioid receptors in the brain?
-Periaqueductal gray (PAG) - locus ceruleus - rostral ventral medulla (RVM) -hypothalamus
67
These 2 opioid receptors effects include low abuse potential and miosis?
Mu1 and Kappa
68
These 2 opioid receptors cause physical dependence and constipation?
Mu2 and Delta
69
This opioid receptor is the only receptor that does not produce supraspinal analgesia?
Mu2
70
This opiod receptor causes bradycardia, hypothermia, and urinary retention?
Mu1
71
This opioid receptor can cause dysphoria and diuresis?
Kappa
72
Endorphins, morphine, and synthetic opioids are agonists of these receptors?
Mu1 and Mu2
73
What is the agonist for kappa and delta receptors?
Kappa: Dynorphins Delta: Enkephalins
74
These opioid receptors cause depression of ventilation?
Mu2 and delta
75
What are the CV side effects from opioids?
* Histamine release causing decreased SNS tone in veins = ↓ venous return, CO, and BP * Bradycardia * Increased effects with benzos or nitrous * Cardioprotective from MI
76
What drug can antagonize the ventilatory depression of opiods? How?
* Physostigmine * Increases CNS ACh levels - reducing ventilatory effects while maintaing analgesia
77
What severe side effect of opioids can be exacerbated by mechanical ventilation? Treatment?
- Thoracic and abominal muscle rigidity - can lead to difficulty with ventilation/oxygenation - Tx: muscle relaxant or naloxone ## Footnote Primarily seen with fentanyl and its derivatives, especially sufentanil
78
How can you determine is someone is having biliary pain from opioids or angina?
Give naloxone - biliary pain will improve but angina will not
79
What are all of the drug treatment options for Sphintcter of Oddi spasms?
80
High doses of intra-op opiods can cause ____ post op pain?
Greater Due to hyperalgesia - low dose intraop is preferred
81
Meperidine works on ____ and ____ opioid receptors Its analogues are?
μ and kappa Fentanyl, sufentanil, alfentanil, and remifentanil
82
Lung first pass effect of fentanyl? What does this mean?
* 75% * The lungs act as reservoirs and remove compounds from the pulmonary arterial blood, reducing the concentration of the active drug available to reach its site of action
83
Why is fentanyl's context sensitive half life so high?
Fentanyl saturates inactive tissues - when the infusion is stopped there is a large amount of drug that returns to the plasma
84
Rank the opioids in lecture from most potent to least potent?
sufentanil > fentanyl = remifentanil > alfentanil > hydromorphone > morphine > meperidine > codeine
85
Effect site equilibration best represents what?
Onset of action
86
Explain the ceiling effect?
87
How does butorphanol produce analgesia and anti-shivering effects?
Moderate affinity for kappa receptors
88
What are the generalized side effects of Opioid Agonist-Antagonists?
They are the same as opioid agonists + dysphoric reactions.
89
Nalbuphine is a ____ receptor agonist and is equally potent to ____
Mu Morphine
90
Which agonist antagonist opioid is good to use in patients with cardiovascular dz?
- Nalbuphine - It does not cause an increase in BP, pulm pressures, HR, or atrial pressures
91
Buprenorphine is a ____ receptor agoinst with an affinity ____ than morphine Why can this be a problem?
* Mu * 50x greater * Has a prolonged resistance to naloxone
92
Similar to Nalbuphine, in that they both do not exhibit cardiovascular effects.
Dezocine
93
This opioid antagonist is nonselective for all 3 opioid receptors?
Naloxone
94
Naloxone dosing?
IV: 1 mcg/kg
95
What opioid antagonist works better PO? Uses?
- Naltrexone - Alcoholism
96
Methylnaltrexone uses?
- Promotes gastirc emptyinh and antagonizes N/V - No alteration in centrally mediated analgesia
97
What is the newer, mu-selective PO peripheral opioid antagonist that is used mainly for post-op ileus?
Alvimopan
98
Buprenorphine plus naloxone...
Suboxone
99
Extended release morphine plus naltrexone...
Embeda
100
Oxycodone plus naltrexone...
OxyNal
101
What is the dose change for epidurals compared to spinals?
5x-10x the dose, has to diffuse accross the dura
102
What is the pathway for drugs for epidural uptake?
- Epidural fat → (epidural venous plexus → systemic absorption )→ diffusion across dura → CSF
103
What contributes to cephalad movement of spinal opioids?
- Lipid solubility - Coughing or straining
104
Which drugs tend to have cephalad movements more when given intrathecally?
Morphine > fentanyl and sufentanil Morphine remains in the CSF more and can migrate upwards, whereas fentanyl crosses into the spinal cord ## Footnote Fentanyl is very lipid soluble and diffuses rapidly, not staying in the CSF
105
Cervical CSF peak levels of fentanyl, sufentanil, and morphine?
Fentanyl: minimal Sufentanil: minimal Morphine: 1-5 hours
106
COX-1 or COX-2? Ubiquitous, "physiologic", inhibition is responsible for many adverse effects
COX-1
107
COX-1 or COX-2? Pathophysiologic, expressed at sites of injury, not protective
COX-2
108
Compare COX-2 selective to Nonspecific NSAIDS
- Comparable analgesia - No effect on platelets - Increase in MI and CVA - Dosage ceiling