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Spring 2024 > Pharm > Flashcards

Pharm Flashcards

Exam II

1
Q

A drug that reversibly depresses the activity of the CNS

A

Sedative-Hypnotics

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2
Q

A drug that reduces anxiety and that has sedation as a side effect

A

Anxiolytic

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3
Q

What are Vessel-poor groups? What % of CO do they receive?

A
  1. Bone
  2. Tendon
  3. Cartilage; 2%
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4
Q

Fat recieves how much CO?

A

5%

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5
Q

What muscle groups receive how much CO? What %?

A
  1. Skeletal muscle
  2. Skin; 18%
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6
Q

What are the vessel-rich groups? What % of CO do they receive?

A
  1. Brain
  2. Heart
  3. Kidney
  4. Liver ; 75%
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7
Q

What are the 4 stages of general anesthesia?

A
  1. Analgesia
  2. Delirium
  3. Surgical Anesthesia
  4. Medullary Paralysis
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8
Q

What are the 5 components of general anesthesia?

A
  1. Hypnosis
  2. Analgesia
  3. Muscle Relaxation
  4. Sympatholysis
  5. Amnesia
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9
Q

It starts with the initiation of an anesthetic agent and ends with the loss of conciousness

A

Stage 1: Analgesia

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10
Q

It starts with the loss of consciousness to the onset of automatic rhythmicity of vital signs.

A

Stage 2: Delirium

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11
Q

It starts with the absence of response to surgical incision and depression in all elements of nervous system function.

A

Stage 3: Surgical Anesthesia

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12
Q

It starts with cessation of spontaneous respiration and medullary cardiac reflexes.

A

Stage 4: Medullary Paralysis

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13
Q

The lightest level of anesthesia

A

Stage 1: Analgesia

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14
Q

Rapid stage that is chracterized by excitement, movements, laryngospasm, and emesis

A

Stage 2: Delirium

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15
Q

Stage associated with flaccid paralysis, absent reflexes, and marked hypotension with a weak, irregular pulse

A

Stage 4: Medullary Paralysis

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16
Q

What are the 4 induction drugs?

A
  1. Barbituates
  2. Propofol
  3. Etomidate
  4. Ketamine
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17
Q

What drug is the gold standard for comparison with other drugs?

A

Barbituates

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18
Q

What is the MoA of Barbituates?

A

Potentiate GABAA channel activity; directly mimics GABA

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19
Q

What other receptors do barbituates work on besides GABAA?

A
  1. Glutamate
  2. Adenosine
  3. Neural nACh
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20
Q

Barbiturates are cerebral vaso_____. They ______ CBF and ______ CRMO2 by 55%

A

vasoconstrictors; decrease; decrease

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21
Q

Barbituates have a lengthy…

A

context-sensitive half-time

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22
Q

Barbiturates have a ____ onset & _____ awakening d/t ____ uptake and ____ redistribution

A

rapid; rapid; rapid; rapid

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23
Q

How are barbituates dosed?

A

Dosed on LEAN body weight

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24
Q

What is the primary metabolism mechanism for barbituates?

A

Liver Hepatocytes

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25
Q

What drug is given rectally with uncooperative/young patients?

A

Barbituates

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26
Q

Which barbituates are the thiobarbituates?

A
  1. Thiopental
  2. Thiamylal
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27
Q

Which barbiturates are the oxybarbiturates?

A
  1. Methohexital
  2. Phenobarbital
  3. Pentobarbital
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28
Q

What is the dose for Thiopental (Sodium Pentothal)? How is the dose calculated?

A

4 mg/kg IV; IBW

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29
Q

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

A

Partition Coefficients

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30
Q

Describes the distribution of an anesthetic between blood and gas at the same partial pressure

A

Blood-gas coefficient

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31
Q

Which barbiturates have oxygen in the second position?

A

Oxybarbiturates

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32
Q

What gives thiobarbiturates more hypnotic potency and lipid solubility?

A

Sulfur atom in place of the oxygen atom in the second position.

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33
Q

What are two side effects of methohexital?

A
  1. Myoclonus
  2. Hiccoughs
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34
Q

What is the dose for Methohexital (Brevital)

A

1.5 mg/kg IV

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35
Q

What are the primary CV effects of barbiturates?

A
  1. Lack of baroreceptor response
  2. Histamine release - anaphylactoid response with previous exposure
  3. Transient decreases in BP
  4. Trainsent increase in HR
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36
Q

What are the primary respiratory effects of barbituates?

A

Dose-dependent depression of ventilatory centers

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37
Q

Results in immediate, intense vasoconstriction and excruciating pain that radiates along the distribution of the artery

A

Intra-arterial injection of barbiturates

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38
Q

What’s the antidote for an intra-arterial injection of barbiturates?

A

Licodaine or papaverine

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39
Q

What is the MoA for propofol?

A

GABA receptor agonist

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40
Q

What’s the induction dose for propofol?

A

1.5-2.5 mg/kg IV

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41
Q

What’s the conscious sedation dose of propofol?

A

25-100 mcg/kg/min

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42
Q

What is the constitution of a 1% solution of propofol?

A
  1. Soybean oil (10%)
  2. Glycerol (2.25%)
  3. Purified egg phosphatide (1.2%)
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43
Q

What are the 3 primary disadvantages of propofol?

A
  1. Support bacterial growth
  2. Causes increased plasma triglyceride concentrations
  3. Pain on injection
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44
Q

What happens when propofol binds to a GABAA receptor?

A

Transmembrane chloride conductance increases

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45
Q

What is the elimination 1/2 time of propofol?

A

0.5-1.5 hours

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46
Q

A low lipid emulsion with no preservative and higher incidence of pain on injection.

A

Ampofol

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47
Q

What are 3 potential contraindications or precautions with propofol use?

A
  1. Cirrhosis of the liver
  2. Renal dysfunction
  3. Pregnancy and the neonate
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48
Q

What are the two primary uses for propofol?

A
  1. Induction
  2. TIVA
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49
Q

Why do children require a higher dose of propofol?

A

Larger central distribution volume and faster clearance rate

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50
Q
  1. Minimal analgesic and amnestic effects
  2. Prompt recovery without residual sedation
  3. Low incidence of PONV
  4. Anticonvulsant
  5. Bronchodilation
A

Benefits of propofol

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51
Q

What are two notable case types that benefit from propofol use?

A
  1. Agent of choice in GI endoscopy procedures
  2. Mechanically ventilated patients in the ICU or postop (cardiac, neuro, etc.)
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52
Q

What is the MoA for propofol’s antiemetic effects?

A

It depresses subcortical pathways and has a direct depressant effect on the vomiting center

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53
Q

What’s the sub-hypnotic dose of propofol? Anti-pruritic?

A

10-15 mg IV followed by 10mcg/kg/min; 10mg

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54
Q

What are the 3 primary CNS effects of propofol?

A
  1. Decreases CRMO2, CBF, and ICP
  2. Larger doses decrease CPP
  3. Myoclonus
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55
Q

How does propofol cause its vasodilatory effects?

A

Inhibition of the SNS and decreases intracellular Ca2+

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56
Q

What does the green and cloudy urine from propofol come from?

A
  1. Phenols (Green)
  2. Uric acid crystallization (Cloudy)
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57
Q

What are two severe side effects of propofol?

A
  1. Profound bradycardia and asystole in healthy adult patients
  2. Severe, refractory, and fatal bradycardia in children
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58
Q

What causes pain at the injection site with etomidate?

A

Propylene glycol

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59
Q

What’s the onset for Etomidate?

A

1 min

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60
Q

What’s the dose for Etomidate?

A

0.3mg/kg

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61
Q

What’s the MoA for Etomidate?

A

Selective modulator of GABAA receptors

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62
Q

What is the best patient population to use Etomidate with?

A

Patient’s with unstable CV system

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63
Q

What are two of the primary side effects of Etomidate?

A
  1. Myoclonus
  2. Adrenocortical Suppression
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64
Q

How often does myoclonus happen in patients given Etomidate?

A

50-80%

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65
Q

What are two contraindications to using etomidate?

A
  1. Sepsis
  2. Hemorrhage
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66
Q

How is Etomidate metabolized?

A

Hydrolysis by hepatic microsomal enzymes and plasma esterases

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67
Q

What happens with adrenocortical suppression?

A
  1. No stress response (no cortisol)
  2. Enzyme inhibition for 4-8 hours
  3. Severe hypotension
  4. Longer mechanical ventilation
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68
Q

Fentanyl 50mcg/mL is available. Patient is 75kg. Administer 1mcg/kg to attenuate myoclonus. How many mLs will you administer?

A

1.5 mLs

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69
Q

What is ketamine a derivative of?

A

PCP

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70
Q

It resembles a cataleptic state in which eyes remain open with a slow nystagmic gaze. The patient is uncommunicative, but wakefulness is present. Purposeful movement.

A

Dissociative anesthesia

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71
Q

What is the preservative in ketamine?

A

Benzethonium Chloride

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72
Q

What is the MoA for Ketamine?

A

Inhibit uptake of catecholamines back into the postganglionic sympathetic nerve endings

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73
Q

What receptors to ketamine bind to?

A

N-Methyl-D-aspartate (NMDA) receptors

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74
Q

What is the most abundant excitatory neurotransmitter in CNS?

A

Glutamate

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75
Q

What are the pharmacokinetics of Ketamine?

A
  1. Rapid onset
  2. Short duration of action
  3. Large Vd - highly lipid soluable
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76
Q

How long does ketamine last?

A

10-20 minutes

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77
Q

When is ketamine’s peak plasma concentration?

A

1 minute

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78
Q

What is norketamine?

A

Active metabolite of Ketamine (1/3 potency)

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79
Q

What is the induction dose for ketamine?

A

0.5-1.5 mg/kg IV

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80
Q

What is the subanesthetic dose for Ketamine?

A

0.2-0.5 mg/kg IV

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81
Q

What induction drug has weak actions at GABAA receptors?

A

Ketamine

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82
Q

Besides NMDA, what are the other receptors that Ketamine works on?

A
  1. Mu
  2. Kappa
  3. Delta
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83
Q

What are the neuraxial doses of Ketamine?

A

30 mgs Epidural
5-50 mg in 3mLs of saline intrathecal/spinal

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84
Q

Ketamine 25mgs/mL is available. How much diluent should be used to decrease the concentration to 5mgs/mL?

A

4 mLs

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85
Q

What is the coronary artery disease cocktail?

A
  1. Diazepam 0.5mg/kg IV
  2. Ketamine 0.5 mg/kg IV
  3. Continuous ketamine infusion mcg/kg/min
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86
Q

What are some of the nonanesthesia clinical uses for ketamine?

A
  1. Burn dressing, debridement, grafting
  2. Psychiatric disorders
  3. Reversal of opioid tolerance
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87
Q

What are the contraindications for ketamine?

A
  1. PHTN
  2. Increased ICP
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88
Q

What are some issues ketamine can cause during induction? How are they prevented/treated?

A

Coughing and laryngospasm; give an antisialoagogue or Glycopyrrolate

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89
Q

With Ketamine ventilatory response to CO2is ___________ .

A

maintained/unchanged

90
Q

Ketamine is a potent cerebral vaso________.

A

Vasodilator

91
Q

What should be given 5 minutes before emergence in patients at risk for emergence delirium from ketamine?

A

Benzodiazepine

92
Q

This induction agent has the highest analgesic properties.

A

Ketamine

93
Q

Combining, admixing, diluting, pooling, reconsitutring, repackaging, or otherwise altering a drug or bulk drug substance to create a sterile preparation.

A

Sterile Compounding

94
Q

The experience of pain with a series of complex neurophysiologic processes

A

Nociception

95
Q

What are the two components of pain?

A
  1. Sensory-discriminative - preception
  2. Motivational-affective - response to pain
96
Q

Increased pain sensations to normally painful stimuli

A

Hyperalgesia

97
Q

Allodynia

A

Perception of pain sensations in response to normally non-painful stimuli

98
Q

Nerve/electrical impulses/signals start at the nerve endings

A

Transduction

99
Q

Travel of nerve/electrical impulses to the nerve body connecting to the the dorsal horn of the spinal cord.

A

Transmission

100
Q

Process of altering (inhibitory/excitatory) pain transmission mechanisms at the dorsal horn to the PNS and CNS.

A

Modulation

101
Q

Thalamus acting as the central relay station for incoming pain signals and the primary somatosensory coretex serving for discrimination of specfic stimuli

A

Preception

102
Q

Where does the modulation of pain impulses occur?

A

Dorsal Horn

103
Q

Chemical Mediators
PELNCCE

A
  1. Peptides (Substance P, Calcitonin, Bradykinin, CGRP)
  2. Eicosanoids
  3. Lipids (Prostaglandins, Thromboxanes, Leukotrienes, Endocannabinoids)
  4. Neutrophils
  5. Cytokines
  6. Chemokines
  7. Extracellular proteases and protons
104
Q

At the original site of injury from heat and mechanical injury

A

Primary Hyperalgesia

105
Q

Pain sensation from uninjured skin surrounding the actual injury (only from mechanical stimuli)

A

Secondary hyperalgesia

106
Q

Pain is not felt with simultaneous inhibitory impulses

A

Gate Closed

A beta fibers

107
Q

Pain is projected to supraspinal brain regions

A

Gate open

A delta & C fibers

108
Q

Which lamina is the substantia gelatinosa? What affects this pathway?

A

Lamina II; Opiates and afferent C-fibers

109
Q

Which lamina is the marginal layer? Which fibers use this pathway?

A

Lamina I; C-fibers

110
Q

What lamina has the NKI receptor? What activates this receptor?

A

Lamina III & IV; Substance P

111
Q

What structures depress or facilitate the integration of pain info in the spinal dorsal horn?

A

Periaqueductal gray-rostral ventromedial medulla (PAG-RVM)

112
Q

What are the 5 excitatory impulses?

GCNAS

A
  1. Glutamate
  2. Calcitonin
  3. Neuropeptide Y
  4. Aspartate
  5. Substance P
113
Q

What are the 5 inhibitory impulses?

GGEND

A
  1. GABA
  2. Glycine
  3. Enkephalins
  4. Norepinephrine
  5. Dopamine
114
Q

What are the two descending pathways of pain modulation?

A
  1. Descending inhibition pathway
  2. Descending facilitation pathway
115
Q

What are the 4 ascending pathways of nociceptive information?

A
  1. Spinothalamic - pain, temp, itch
  2. Spinomedullary
  3. Spinobulbar
  4. Spinohypothalamic - autonomic
116
Q

When do neonates start to feel pain?

A

23 weeks of gestation

117
Q

What are the receptors for the PAG-RVM system?

A

μ, κ, δ

118
Q

What type of pain persists after the tissue has healed? Cancer patients have an increased risk for this type of pain.

A

Neuropathic

Will also see allodynia and hyperalgesia with this type pain.

119
Q

What is the GI response to pain?

A

N/V

120
Q

What are the emotional responses to pain?

A
  1. Anxiety
  2. Sleep disturbance
  3. Depression
121
Q

What are the immune responses to pain?

A
  1. Leukocytosis- stress related
  2. Depressed reticuloendothelial system - increased infection
122
Q

What are the 4 advantages of opioid agonist-antagonists?

A
  1. Analgesia
  2. Limited ventilation depression
  3. Low potential for physical dependence
  4. Ceiling effect prevents additional responses
123
Q

When are opiod agnists-antagonists used?

A

When a patient is unable to tolerate a pure agonist

124
Q

What is the MoA for opioid agonists-antagonists?

A
  1. μ - partial (agonist) or no effect (competitive antagonist)
  2. κ, δ - partial effect (agonist)
125
Q

Which opiod agonist-antagonist has withdrawal as a side effect?

A

Burenorphine

126
Q

Which opioid agonist-antagonist is used with cardiac catheterization patients?

A

Nalbuphine

127
Q

Which opioid agonist-antagonist has effects on the κ, δ receptors with weak antagonist activity and excretion via glucoronide conjugates?

A

Pentazocine

128
Q

Pentazocine
Butorphanol
Nalbuphrine
Buprenorphine
Nalorphine
Bremazocine
Dezocine

are all examples of what type of opioids?

A

Opioid agonists-antagonists

129
Q

Which opioid agonist-antagonist is more potent than morphine?

A

Buprenorphine

130
Q

Which opioid agonist-antagonist has affinity for all three opioid receptors?

A

Butorphanol
δ - minimal affinity
μ - low affinity
κ - moderate affinity

131
Q

What are the 3 opioid antagonists?

A

Naloxone
Naltrexone
Nalmefene

132
Q

What are two other uses for Naloxone?

A
  1. Neonate
  2. Antagonism of general anesthesia at high doses
133
Q

How long does Naloxone last?

A

30 to 45 minutes

134
Q

What is the MoA of opioid antagonists?

A

Pure μ opioid receptor competitive antagonists with no agonist activity.

135
Q

Name three S/E of Naloxone.

A
  1. Reversal of analgesia (not a side effect…)
  2. N/V
  3. Increased SNS (HR, BP, pulmonary edema, arrythmias)
136
Q

What kind of medications are suboxone, Embeda, and OxyNal?

A

Tamper or abuse resistant opioids
1. Suboxone (buprenorphine + naloxone)
2. Emebda (ER morphine + naltrexone)
3. OxyNal (oxycodone + naltrexone)

137
Q

What medication decreases MAC? How much of a decrease?

A

Fentanyl; decreases MAC of Iso and Des by 50%

138
Q

What structure/pathway in the spinal cord contains opioid receptors?

A

Substantia Gelatinosa

139
Q

What are the neuraxial routes for opioids?

A
  1. Epidural
  2. Spinal
  3. Intrathecal
  4. Subarachnoid
140
Q

What does adding epinephrine to epidurals help prevent?

A

Venous plexus injuries

141
Q

What are the peak concentrations in epidurals for Fent, Sufent, and Morphine?

A

Sufent - 6 minutes
Fent - 20 mimnutes
Morphine - 1-4 hours

142
Q

What causes itching with neuraxial opioids?

A

Cephalad (head or anterior end of the body) migration of the opioid to trigeminal nucleus

143
Q

What determines cephalad movement of opioids in the CSF?

A

Lipid solubility

144
Q

Which drug is used to attenuate the side effects of neuraxial opiods?

A

Naloxone

145
Q

Which opiates are phenanthrenes?

A
  1. Morphine
  2. Codeine
  3. Thebaine
146
Q

Greek word stupor, which has the potential to produce physical dependence

A

Narcotic

147
Q

All exogenous substances (natural & synthetic)

A

Opioid

148
Q

In addition to opiate receptors, where else do opiates have an effect?

A

Pre & postsynaptic sites in the CNS

149
Q

Opiates have ____synaptic inhibition of what substances?

A

pre; ACh, dopa, NE, Substance P

150
Q

Where are the opioid receptors in the brain?

A
  1. Periaqueductal gray (PAG)
  2. Locus ceruleus
  3. rostral ventral medulla (RVM)
  4. Hypothalamus
151
Q

Where are the opioid receptors in the spinal cord?

A

Interneurons and primary afferent neurons in the dorsal horn (substantia gelatinosa)

152
Q

Where are the opioid receptors outside of the CNS?

A

sensory neurons and immune cells

153
Q

What is the CV benefit of opioids?

A

cardioprotective from myocardial ischemia

154
Q

What is the primary CV side effect of opioids?

A

Decreased SNS tone in peripheral veins (decreases VR, CO, & BP, orthostatic hypotension & syncope), bradycardia

155
Q

Which medication increases CNS levels of ACh and antagonizes ventilatory depression, but not analgesia?

A

Physostigmine

156
Q

What is the MoA for decreased ventilation with opiates?

A
  1. Activation of Mu2 receptors which decrease ventilation rate with a compensatory increase in tidal volume
  2. Increased in resting PaCO2
157
Q

What are symptoms of opioid overdose?

A

Hypoventilation, miosis apnea, & coma

158
Q

What’s a contraindication for opiates?

A

Head injury

159
Q

What are 3 CNS side effects of opioids?

A
  1. Myoclonus with large doses
  2. Thoracic and abdominal muscle rigidity
  3. Decreased CBF and possibly ICP
160
Q

What 3 opiates cause spasm of biliary smooth muscle or sphincter of Oddi spasms?

A
  1. Fentantyl
  2. Morphine
  3. Meperidine
161
Q

What medication is given for patients with biliary smooth muscle spasms?

A

Glucagon (2 mgs IV - given incrementally)

162
Q

What is the primary GI side effect of opioids?

A

Delayed gastic emptying and constipation

163
Q

What are the initial symptoms of opioid withdrawal?

A

Yawning, diaphoresis, lacrimation, insomnia, restlessness, coryza

164
Q

What is the onset time for fentanyl, sufentantil, and remifentantil?

A

30-60 seconds

165
Q

What are the two metabolites of morphone?

A
  1. Morphine-3-glucuronide (inactive)
  2. Morphine-6-glucuronide (active)
166
Q

What type of pain is morphine best at?

A

dull pain

167
Q

What is the normal dose for morphine?

A

1-10mg IV

168
Q

What is the normal onset for morphine?

A

10-20 minutes

169
Q

What is the peak time for morphine?

A

15-30 minutes

170
Q

Which morphine metabolite has a longer elimination 1/2 time?

A

Morphine-3-Glucuronide
caution with renal dysfunction

171
Q

Which receptors does meperidine work on?

A

Mu and kappa

172
Q

What are the 4 analogues of mepridine?

A
  1. Fentanyl
  2. Sufentanil
  3. Alfentanil
  4. Remifentanil
173
Q

What’s the dose for post-op shivering with meperidine?

A

12.5 mgs

174
Q

What is the duration of meperidine? What is the elimiation 1/2 time?

A

2 to 4 hours; 3 to 5 hours

175
Q

What is the induction dose of fentantyl?

A

1.5 to 3 mcg/kg IV

176
Q

What is the analgesic dose of Fentanyl

A

1-2 mcg/kg IV

177
Q

What’s the induction dose of remifentanil?

A

0.5 to 1 mcg/kg IV over 30-60 seconds

178
Q

What is the maintainence dose of remifentanil?

A

0.005 to 2 mcg/kg/min

179
Q

What can using alfentanil with alzheimer patients cause?

A

acute dystonia

180
Q

What is the dose of hydromorphone?

A

0.5 mg IV (1 to 4 mgs total)

181
Q

What is the cough suppressant dose of coedine?

A

15 mgs

182
Q

What receptors does tramadol work on?

A

Mu, weak kappa, and delta.

183
Q

What’s the chemical ring in most opioids?

A

Piperdine

184
Q

What is the dose for super mag?

A

400 mg

185
Q

What is the dose for IV tylenol?

A

1000mg q4-6 hours.

186
Q

What is the intraop dosage for ibuprofen?

A

200-800 mg IV over 30 minutes Q6h

187
Q

What are the chronic pain syndromes gabapentin can be used for?

A
  1. Diabetic neuropathy
  2. Post-herpetic neuralgia
  3. Reflex sympathetic dystrophy
  4. Phatom limb pain
  5. Fibromyalgia
188
Q

What are the two primary indications for gabapentin?

A
  1. Partial seizures in adults/children
  2. chronic pain syndromes
189
Q

What’s the MoA for gabapentin?

A
  1. Binds VG-Ca2+channels
  2. Enhances descending inhibition
  3. Inhibits excitatory NT release
190
Q

What’s the dose for gabapentin?

A

300-1200mg PO 1-2 hours prior to OR

191
Q

When is Gabapentin contraindiciated?

A
  1. MG
  2. Myoclonus

Reduce dose in elderly.

192
Q

What are some of the benefits of NSAIDs?

A
  1. Long duration of action
  2. Prepemptive analgesia
  3. Less N/V
  4. Abscense of cognitive effects
  5. No addictive potential
  6. No respiratory depression
193
Q

What do NSAIDs do?

A
  1. Analgesic (Decrease activation of peripheral nociceptors)
  2. Antiinflamatory
  3. Antipyretic
194
Q

What medications are the nonspecific NSAIDs?

A
  1. Ibuprofen
  2. Naproxen
  3. Aspirin
  4. Acetaminophen
  5. Ketorolac
195
Q

What are the COX-2 Selective NSAIDs?

A
  1. Celecoxib (Celebrex)
  2. Rofecoxib (Vioxx)
  3. Valdecoxib (Bextra)
  4. Parecoxib (Dynastat)
196
Q

What’s the dose for Celebrex?

A

200 to 400mg PO QD

197
Q

What is the enzyme that catalyzes synthesis of PG?

A

Cyclooyxgenase

198
Q

Ubiquitous, “physiologic”, “Constituative”

A

COX-1

199
Q

“Inducible”, “pathophysiologic”, sensitization

A

COX-2

200
Q

What’s the dose for ketorolac?

A

15-30mg q6hr

1/2 dose in elderly

201
Q

What is the peak for IV tylenol?

A

30 minutes to 1 hour

202
Q

What is the TEAM health forumla for Ketamine?

A
  1. 0.25 to 0.5 mg/kg pre incision
  2. 0.25 to 0.5 mg/kg intraop
  3. Stop 1 hour prior to surgery end
  4. 0.12 mg/kg/hr for 24 hours postop

or 5mg boluses between 0.3 to 0.5 mg/kg/hr

203
Q

What’s the dose for lidocaine?

A

1-2 mg/kg IV over 2-4 minutes

204
Q

What’s the TEAM health dose for Lidocaine?

A
  1. 1.5 mg/kg at induction
  2. 1-2 mg/kg/hr for 24 to 48 hours post-op
205
Q

What dose of lidocaine corresponds to analgesia?

A

1-5 mcg/mL

206
Q

What dose of lidocaine corresponds to tinnitus, muscle twitching, hypotension, myocardial depression, and oral numbness

A

5-10 mcg/mL

207
Q

What dose of lidocaine corresonds to seizures and unconciousness?

A

10-15 mcg / mL

208
Q

What dose of lidocaine corresponse to apnea and coma?

A

15-25 mcg/mL

209
Q

What dose of lidocaine corresponds to cardiovascular depression?

A

> 25 mcg/mL

210
Q

What is the primary contraindication for Ketorolac (Toradol)?

A

Severe renal impairment

211
Q

What’s the peak time for celebrex?

A

3 hours

212
Q

What’s the team health dose of Mg2+

A

30 to 50 mg/kg IV loading dose
Continue 8 to 10 mg/kg/hr

213
Q

What’s the preop dose for Mg2+

A

50 mg/kg IV

214
Q

What decreases ondansetron effectiveness?

A

Variations in CYP2D6 activity

215
Q

What’s the dose for ondansetron?

A

4 mg to 8mg IV

216
Q

What’s the dose for pediatric ondansetron?

A

0.1 mg/kg IV

217
Q

What medications do corticosteroids increase the effectiveness of?

A

Increases effectiveness for 5-HT3 antagonists and droperidol

218
Q

What is the dose for decadron?

A

8 to 10 mgs?

219
Q

What endogenous substances are peptides?

SCBC

A

Substance P, Calcitonin, Bradykinin, and CGRP

220
Q

What endogenous substances are lipids?

PTLE

A

Prostaglandins, Thromboxanes, Leukotrienes, and Endocannabinoids

Spring 2024 (9 decks)

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