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N926 Pharmacology > 21 Fall Pharm Final Oral > Flashcards

21 Fall Pharm Final Oral Flashcards

1
Q

Desflurane VP

A

669mmHg

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2
Q

Desflurane MAC

A

6%

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3
Q

Desflurane B:G

A

0.42

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4
Q

Desflurane O:G

A

19

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5
Q

volatile agents MOA

A

Unknown – likely involves NMDA receptors, tandem pore K+ channels, VG-Na+ channels, glycine receptors, and GABA receptors in the cerebral cortex, brain stem arousal centers, central thalamus, and spinal cord.

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6
Q

Isoflurane MAC

A

1.2%

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7
Q

Isoflurane VP

A

238mmHg

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8
Q

Isoflurane B:G

A

1.4

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9
Q

Isoflurane O:G

A

91

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10
Q

Sevoflurane MAC

A

2%

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11
Q

Sevoflurane B:G

A

0.68

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12
Q

sevolurane O:G

A

50

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13
Q

sevoflurane VP

A

157mmHg

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14
Q

Nitrous Oxide MAC

A

104%

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15
Q

Nitrous Oxide O:G

A

1.4

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16
Q

Nitrous Oxide B:G

A

0.47

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17
Q

Nitrous Oxide VP

A

38770

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18
Q

What is the MOA of magnesium?

A

Mag works in opposite direction of calcium, calcium excites, mag inhibits

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19
Q

The 3As in anesthesia and which location in the brain.

A

amnesia (brainstem), analgesia (thalamus), and areflexia (spinal cord) (no SNS/PSNS changes in V/S)

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20
Q

How to treat MH?

A

Na+ dantrolene 1.5 mg/kg or Ryanodex

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21
Q

Stages of anesthesia

A

Stage I – Amnesia & Anesthesia

Stage II – Delirium & Excitation

Stage III – Surgical Anesthesia

Stage IV – Anesthetic overdose

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22
Q

In what population should you avoid using desflurane?

A

Stinky bad boy!!! Avoid in patients with reactive airway disease

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23
Q

Which inhalational agent is best for inhalational induction

A

Sevoflurane

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24
Q

What complication can sevoflurane produce? How to mitigate? Surgery implication?

A

If used with Lyme, can create nephrotoxic compound A. Use lime can reduce risk. Give flow >2lpm

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25
Q

What is this?

A

desflurane

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26
Q

What is this

A

isoflurane

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27
Q

what is this?

A

Sevoflurane

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28
Q

Wha is special about Isoflurane?

A

Most potent, slowest. concern for coronary steal in HoTN

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29
Q

What are contraindications of nitrous oxide?

A
  • methionine synthase pathway deficiency
  • surgery involving gas filled spaces
    • middle ear
    • pneumothorax
    • intraocular air bubble
    • 1st tremester
    • increased ICP
    • long cases > 6hr
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30
Q

The ideal anesthetic agent

A
  • Non-irritating to the respiratory tract
  • Rapid induction and emergence
  • Chemically stable (non-flammable)
  • Produce amnesia, analgesia and areflexia
  • Potent
  • Not metabolized and excreted by respiratory tract
  • Free of toxicity and allergic reactions
  • Minimal systemic changes
  • Uses a standardized vaporizer
  • Affordable
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31
Q

Is propofol an acid or a base?

A

Acid

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32
Q

Propofol induction dose?

A

1.5mg/kg-2.5mg/kg

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33
Q

Propofol MAC (endoscopy) dose

A

25-100 mcg/kg/min

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34
Q

Propofol TIVA dose?

A

100mcg-300mcg/kg/min

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35
Q

Propofol antiemetic dose?

A

10mg IV

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36
Q

Propofol antipruritic dose?

A

10mg IV

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37
Q

Propofol anticonvulsive dose?

A

1mg/kg IV

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38
Q

Propofol MOA

A

GABA modulator (allosteric) – Cl- influx hyperpolarizes neuron (IPSP).

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39
Q

Propofol t1/2

A

30min - 1hr

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40
Q

Propofol Vd

A

2.5-3.5

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41
Q

Propofol active metabolites

A

4- hydroxypropofol

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42
Q

What’s propofol’s biggest advantage?

A

Rapid return to consciousness with minimal residual effect

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43
Q

Unique about propofol metabolism

A

Clearance exceeds hepatic blood flow (liver)

Tissue uptake in the lungs

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44
Q

Propofol context sensitive t1/2

A

<40 min

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45
Q

Factors that affectd FA/FI

A

Factors that affect the FA/FI ratio include:

  • the delivered inspired anesthetic concentration,
  • the blood-gas partition coefficient of the inhalation agent,
  • alveolar ventilation (VA),
  • cardiac output (Qt),
  • and the distribution of Q to the vessel-rich organs (i.e., heart, brain, kidneys, and liver).
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46
Q

Etomidate MOA

A

GABA modulator

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47
Q

What does GABA stand for?

A

Gamma-aminobutyric acid

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48
Q

How long does propofol last?

A

8-10 min

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49
Q

How long does etomidate last?

A

5-15 min

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50
Q

Contraindication of etomidate

A

Porphyria, septic shock (etomidate causes suppressed 11-betahyroxylase for 8 hrs, low cortisol)

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51
Q

How is etomidate metabolized?

A

hydrolysis, plasma esterase and microsomal enzymes in the liver.

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52
Q

Etomidate induction dose

A

0.2-0.4mg/kg IV

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53
Q

Is Etomidate an acid or base?

A

It’s a base.

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54
Q

Etomidate t1/2

A

2-5 hrs

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55
Q

Ketamine induction dose

A

1-2.5mg/kg

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56
Q

ketamine t1/2

A

2-3 hrs

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57
Q

Etomidate VD

A

2.2-4.5

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58
Q

Ketamine Vd

A

3.5-4.5

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59
Q

Ketamine MOA

A

NMDA (N-methyl-D-aspartate) non-competetive antagonist ==> dissociative amnesia

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60
Q

Ketamine dart dose, onset time

Ketamine PO dose, onset time

A

dart 4-8mg/kg, <10 min onset

PO 10 mg, 10-20 min onset

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61
Q

Ketamine active metabolite

A

metabolized by liver, norketamine

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62
Q

ketamine contraindication

A

increased ICP

eye procedures

eye trauma

high emergence delirium risk

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63
Q

benzodiazepine MOA

A

allosteric agonist on GABA

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64
Q

benzodiazepine effects

A

anxiolytic

muscle relaxant

anticonvulsant

anterograde amnesia

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65
Q

What are side effect of benzodiazepine?

A

STRONG synergistic effect with opioids (RESPIRATORY DEPRESSION)!!!

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66
Q

midazolam induction dose

A

0.02-0.04mg/kg

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67
Q

midazolam Vd

A

High

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68
Q

How is midazolam metabolized? active metabolite?

A

rapid metabolism in liver d/t imidazole ring.

active metabolite:

  • 1-hydroxymidazolam, which has half the activity
  • 4- hydroxymidazolam, nondetectable amount
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69
Q

midazolam t1/2

A

2 hrs

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70
Q

Is midazolam injection painful? why?

A

water soluble with imidazole ring. only benzo with painless injection

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71
Q

Is midazolam an acid or base?

A

Base

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72
Q

Is diazepam Vd?

A

High

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73
Q

diazepam t1/2

A

>40 hrs

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74
Q

How is diazepam metabolized? Active metabolites?

A

Liver I (oxidative)

Active metabolites:

  • desmethyl diazepam (responsible for long t1/2)
  • Oxazepam
  • temazepam
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75
Q

diazepam contraindication

A

don’t give to pt with porphyria

t1/2 is pt’s age, careful with old pt.

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76
Q

what can diazepam be used for?

A

DT, anticonvulsant, pt with tetany, lumbar disc disease.

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77
Q

Lorazepam t1/2

A

14 hrs

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78
Q

What is special about lorazepam’s PK?

A

Slowest onset (1-2 min) but most potent

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79
Q

What do you use to reverse benzodiazepine?

A

flumazenil

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80
Q

dosage of flumazenil

A

give 0.2mg initially, usually have effect in 2 min.

then give 0.1mg every 60 seconds. 0.5-1mg should completely reverse. if given 5mg and pt still not responsive, something else is going on.

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81
Q

Barbiturates MOA

A

GABA agonist,

also works on adenosine, nAchR, glutamate

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82
Q

barbiturates contraindication

A

Do not give pt with porphyria

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83
Q

What drug should not given to pt with porphyria?

A

Barbiturates

Diazepam

Etomidate

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84
Q

If barbiturates are infused arterially, what to do?

A

papaverine, heparinization, arteriodilate with regional anesthesia

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85
Q

Thiopental induction dose?

A

2.5-5mg/kg

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86
Q

how is Thiopental metabolized? Acftive metabolite?

A

Liver I phase I

Active metabolite: pentobarbital

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87
Q

Thiopental Vd?

A

Large

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88
Q

What is methohexital induction dose?

What is methohexital pediatric dose?

A

1-2mg/kg

25mg/kg

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89
Q

what is methohexital used for?

A

ECT to lower seizure threshold

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90
Q

Opioid MOA

A
  • Pre synaptic – inhibit release of acetylcholine, dopamine, norepinephrine and Substance P
  • Post synaptic – increased K+ conductance = decreased function
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91
Q

opioids major side effects

A
  • CV – bradycardia, impaired SNS response, orthostatic hypotension, SYNERGISM ↓↓ BP with benzos and nitrous oxide!!!
  • Resp – ↓↓ responsiveness to CO2, deep, slow breaths. ↑↑ airway resistance.
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92
Q

Signs of opioid OD

A

miosis+hypoventilation+coma

93
Q

How do you reverse opioid? dose? what’s its t 1/2?

A

naloxone, 1-4ug/kg IV, 30-45 min

94
Q

Morphine active metabolite. DOA and potency?

A

morphine-6-glucorinide, longer DOA, 65X potency than morphine

95
Q

What organ dysfunction can cause respiratory depression when morphine is given?

A

renal dysfunction

96
Q

Meperidine (Demerol) mainly used for?

A

Anti-shivering postoperatively

• Stimulation of kappa receptors

97
Q

Meperidine potency compared to morphine

A

1/10

98
Q

meperidine active metabolite

A

normeperidine

99
Q

normeperidine elimination t1/2

A

15 hrs, >30 hrs in renal failure, accumulation can lead to meperidine delirium, seizures

100
Q

Meperidine Vd

A

High

101
Q

fentanyl induction dose. why use it?

A

1-3 ug/kg

Blunt sympathetic stimulation to intubation

102
Q

are all IV opioids acids or bases?

A

They are bases

103
Q

fentanyl Vd

A

High

104
Q

How is fentanyl metabolized

A

Liver, phase 1

105
Q

Fentanyl context sensitive t1/2 increases after infusion for how long?

A

After 2 hrs. It keeps growing

106
Q

what is responsible for fentanyl’s large first pass uptake?

A

Lungs

107
Q

fentanyl’s potency compared to morphine

A

100x

108
Q

Sufentanyl dose

A

0.1-0.4 u/kg

109
Q

sufentanyl Vd

A

high

110
Q

How is sufentanil metabolized

A

Liver phase I

111
Q

Sufentanil active metabolite

A

desmethyl sufentail

112
Q

Does fentanil release histamine?

A

No

113
Q

What is a big complaint about morphine?

A

Morphine spinals cause crazy itchiness, can cause delayed ventilatory depression

114
Q

Sufentanil potency

A

5-10 x than fentanyl

115
Q

What patient should avoid sufentanil?

A

Renal, accumulation issue

116
Q

What intubation issue can sufentanil cause?

A

Chest wall rigidity

117
Q

Alfentanil dose

A

15mcg/kg

118
Q

What is the biggest advantage of alfentanil

A

fast onset

119
Q

what pt population should avoid alfentanil

A

Avoid in untreated parkinson pt, it causes acute dystonia

120
Q

Remifentanil context sensitive t1/2

A

4 minutes

121
Q

Remifentanil Vd

A

small

122
Q

Remifentanil TIVA dose

A

1-3 ug/kg

123
Q

How is remifentanil metabolized?

A

non specific plasma esterease hydrolysis

124
Q

What do you need to consider when using remifentanil? What do drug could you use?

A

Long acting opioid for postop analgesia. Ketamine (0.5-1mg/kg) and magnesium (1g over 2 hrs) can help

125
Q

What is ketamine mostly used for?

A

Trauma

126
Q

Opioid agonist-antagonist MOA

A

Bind to mu receptors with minimal activation (antagonism) and then bind to kappa/delta for other effects (agonism) àlower efficacy

127
Q

What is butorphanol used for?

A

Good for analgesia, anti-shivering (kappa). Can limit effectiveness of pure opioid agonists though!

128
Q

butorphanol unique side effect

A

dysphoria, hyperdynamic CV (catecholamines)

129
Q

What’s unique about Nalbuphine’s structure?

A

Chemically related to oxymorphone and naloxone; analgesic properties of morphine, 1/4 antagonist of nalorphine

130
Q

how does Nalbuphine’s antagonist effect related to timing?

A

If given before opioid, opioid does not work very well; if given after opioid given, can reverse resp depression for 2-3 hrs but maintain analgesisa

131
Q

Nalbuphine side effects compared with butorphanol

A

compared with Butorphanol less dysphoria, and LIMITED catecholamine stimulation, good for CV patients

132
Q

How does NSAIDS work

A

Damaged cells releases COX and prastaglandins, NSAIDS has anti-inflammatory effect on the damaged nerve endings and reduce inflmmatory response

133
Q

COX-1 fxn

A

maintain renal, GI and thromboxane (PLT aggregation)

134
Q

COX-2 fxn

A

fever, pain, inflammation

135
Q

what type of NSAID is Toradol (Ketorolac)

A

non selective NSAID

136
Q

Ketorolac (Toradol) dose

A

15mg q6h

137
Q

What type of NSAID is Celecoxib?

A

selective Cox-2 inhibitor

138
Q

Benefit and risk fo Celecoxib (Celebrex)

A

less GI toxicity, but increases CV risk

139
Q

Celecoxicb(Celebrex) dose

A

400mg preop, 200mg BID x 5 days postop

140
Q

Are all NSAIDS acids or bases?

A

Acids

141
Q

Do NSAIDS have high Vd or low Vd

A

low Vd

142
Q

NSAIDS are metabolized and eliminated by what?

A

metabolized in liver and eliminated by renal and biliary

143
Q

What can cause hypersensitivity to NSAIDS?

A

nasal polyps + rhinitic allergy + asthma = Risk of anaphylaxis

144
Q

Acetaminophen MOA

A

centrally activate serotonergic pathway, antagonism of NMDA, sub P and nitric oxide pathways

145
Q

Does acetaminophen have anti-inflmmatory effect?

A

No

146
Q

Acetaminophne dosage

A

325-650mg Q4-6h, do not exceed 4000 mg q24h, <2g for chronic alcoholics;

1000mg IV q6h, do not exceed 4000mg/24h

147
Q

What is the NSAID to use in CV patients?

A

Naproxen

148
Q

How does acetaminophen damage liver? How to treat OD?

A

It depletes glutathione.

Charcoal or infusing acytylcisteine

149
Q

Ibuprophen type of NSAID and dose

A

non selective

400-800 mg q6-8h

150
Q

Succynocholine dose

A

1mg/kg

151
Q

How is succinylcholine metabolized

A

PchE

152
Q

Succinylcholine onset

A

60 seconds

153
Q

Succinylcholine DOA

A

9-13 min

154
Q

Atracurium dose

A

0.5 mg/kg

155
Q

Atracurium metabolized

A

Ester hydrolysis and Hoffman

156
Q

Does atracurium have active metabolite?

A

Laudanosine can cause convulsions

157
Q

cisatracurium dose

A

0.1mg/kg

158
Q

cisatracurium metabolized

A

hoffman

159
Q

Explain Succinylcholnine MOA

A

Chemical structure is two Ach molecules connected together, binds to nAchR, cannot be hydrolyzed by AchE, has to drift off into blood stream and metabolized by PchE

160
Q

What populatin is contraindicated for Succinylcholine?

A

Pediatric pt <5 yrs old; hyperkalmelia (will increase K by 0.5); Pt with MH history; ICP issue; eye surgery

161
Q

What is the biggest unfavorable feature of Atracurium? How to treat?

A

Histamine? H1 and H2 blocker.

162
Q

Rocuronium dose

A

0.6mg/kg

163
Q

Rocuronium metabolized

A

Liver and Kidney

164
Q

Rocuronium onset time

A

1.7 min

165
Q

Vecuronium dose

A

0.1 mg/kg

166
Q

Vecuronium metabolized

A

mostly liver, some kidney

167
Q

Vecuronium onset

A

2.4 min

168
Q

Vecuronium active metabolite

A

3-OH (80% potency)

169
Q

pancuroium dose

A

0.08mg/kg

170
Q

pancuronium onset

A

2.9 min

171
Q

pancuronium metabolized

A

major kidney, some liver.

172
Q

What is pancuronium good for?

A

has vagolytic effect, good for CV patient

173
Q

Sugammadex dose

A

>2 twitches 2mg

1-2 twitches 4mg

0 twitches 8-16mg

174
Q

Sugammadex MOA

A

gamma-cyclodextrin encapsulates NMBD (rocuronium)

175
Q

dexmedetomidine dose

A

Preop: 4mcg, up to 20 mcg, monitor for bradycardia

[0.5-1 ug/kg] bolus over 15 minutes, then [0.2-0.7 mcg/kg/hr]; monitor for severe bradycardia (and hypotension)

176
Q

What do you monitor when giving dexmedetomidine

A

bradycardia

177
Q

dexmedetomidine MOA

A

Alpha 2 agonist, inhibits SNS

178
Q

cholinesterase inhibitor MOA

A

inhibit the breakdown of Ach hence increase the concentration of Ach, so they have higher chance of binding to nAchR

179
Q

What is the side effect of cholinesterase inhibitor?

A

muscarinic effect: salvalation, lacrimination, bronchoconstriction, increased bowel motility

180
Q

Edrophonium dose

A

1-1.5 mg/kg

181
Q

What do you pair edrophonium with? Dose?

A

Atropine. 15mcg/kg

182
Q

Neostigmine dose

A

0.06mg-0.08mg/kg

183
Q

What do you pair neostigmine with? Dose?

A

glycopyrrolate, 10-20mcg/kg

184
Q

Scopolamine dose, onset

A

1.5mg behind ears, onset 2-4hrs

185
Q

How to reverse scopolamine? dose and timing?

A

physostigmine, 0.01-0.03mg/kg IV, repeat in 15-30 minutes.

186
Q

Contraindication for scopolamine

A

closed angle glaucoma

187
Q

What are SE of scopolamine?

A

Passes BBB, risk for restless, hallucination->unconsciousness

188
Q

What patient population has highest risk for PONV?

A

Young female, non-smoker, hx of NV, used opioid, motion sickness,

189
Q

Ondasetron MOA. Which area does it work on?

A

5-HT 3 inhibitor, works on chemoreceptor trigger zone.

190
Q

ondansetron dose

A

4mg IV

191
Q

ondansetron which population to adjust dose?

A

hepatic dysfunctional population do not give more than 8mg

192
Q

ondansetron when do you give?

A

30 minutes before end of surgery

193
Q

Major side effect of ondansetron

A

Headache dizziness, prolonged QT

194
Q

Promethazine (Phenergan) dose, preffered route, why?

Onset?

A

12.5-25 IM preffered dt leaking out of vascular space.

onset 5 min IV, 20 min IM

195
Q

promethazine contraindications

A

Older pt>65, causes confusion, give with opioid will cause sedation with opioids

196
Q

Metoclopramide dose

A

10mg

197
Q

metochlopramide MOA

A

dopamine D2 hibitor.

198
Q

metochlopramide dosing adjustment

A

adjust for renal patients.

199
Q

What do you need to be aware of when giving metoclopramide?

A

Slow push, otherwise abd cramping, anxiety

200
Q

metoclopramide contraindication

A

pheochromocytoma, HTN crisis

Don’t give to Parkinson pt d/t EP effects, GI obstruction, seizure

201
Q

what is metoclopramide good for?

A

GI prokinetic

202
Q

What pt population should get corticosteroids

A
  • daily taking >5mg for 2-3 weeks
  • have been on treatment for the last 12 months
203
Q

What can corticosteroids do?

A

anti-inflammatory, immunosuppressant.

204
Q

What do you give during adrenal crisis?

A

Hang fluid NS 1-3L over 1hr, give 100mg hydrocortisone, then 50mg q6h

205
Q

Dexamethasone dose

A

4-10mg IV

206
Q

Contraindication of dexamethasone

A

active infection,

207
Q

What is MAC

A

the minimum alveolar concentration to produce lack of movement in surgery in 50% of populations

208
Q

Factors increasing MAC

A

hyperthermia, alcohol abuse, hypernatremia, increased CNS activity

209
Q

Factors decreasing MAC

A

hypothermia, increased age, pregnancy, alpha 2 agonist, hyponatremia

210
Q

Explain blood gas efficiency

A

the amount of drug that binds to drug(inactive), VS the amount of drug that will diffuse into tissues that has anesthetic effect

211
Q

What is uncoupling effect?

A

CMRO2 decrease, CBF increase

212
Q

why are we using NMBD?

A
  • optimal condition for surgery
  • optimal condition for intubation
  • ventilator synchronization
213
Q

Midazolam pediatric oral dose

A

0.4-0.8 mg/kg

214
Q

Gabapentin preop multimodal pain mgnt dose

Gabapentin postop dose

A

1200mg one time

600mg Q8h x 14 days

215
Q

Lidocaine induction dose. why use it?

Intra op multimodal dose?

A

1mg/kg: to blunt sympathetic stimulation to intubation

1-2 mg/kg/hr

216
Q

Propofol age consideration

A

Decrease dose in elderly; increase in children and young adults

217
Q

When to give dexamethasone

A

give shortly after induction

218
Q

What pt population is contraindicated for ketorolac?

A

avoid renal compromised pt.

219
Q

meperidine antishivering dose?

A

12.5 mg

220
Q

midazolam postop sedation dose? gtt dose

A

0.5-4mg; 1-7mg/hr

221
Q

What mechanism causes miosis?

A

Edinger-westphal nucleus on oculomotor nerve (cranial nerve III)

222
Q

After opioid administration, GI spasm happens at?

A

Sphincgter of oddi

223
Q

What do you do in opioid overdose?

reversal dosage?

A
  • Antagonist
  • Give oxygen
  • mechanical ventilation

Narcan: 1-4 ug/kg IV 5 ug/kg/hr can fix depression of ventilation without affecting analgesia

224
Q

Which pt population should not get atracurium?

A

asthma

225
Q

What is pancuronium not good for?

A

Rapid sequence intubation, due to its slow onset

226
Q

what class of antiemetic is promethazine?

A

Antihistamine

227
Q

What PK property of thiopental makes it different from propofol.

A

10x long elimination t1/2

228
Q

In a perfect world, an indution drug should be:

A
  • rapid smooth onset and recovery
  • analgesia
  • minimal cardiac and respiratory depression
  • antiemetic
  • bronchodilation
  • lack of toxicity and histamine release
  • advantageous pharmocokinetics and pharmaceutics
229
Q

drug doses related to 15

A

ketorolac - 15mg q6h

Alfentanil - 15mcg/kg

Atropine -15mcg/kg

N926 Pharmacology (16 decks)

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