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EB- Advanced Pharm > Exam 1; preop > Flashcards

Exam 1; preop Flashcards

1
Q

Drug effect relates to ____

A

number of bound receptors

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2
Q

Agonists bind through three types of bonds

A

ion, hydrogen, van der waals
and covalent (some do this but we dont like it because we want reversible bonds)

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3
Q

How does competitive antagonism shift the dose response curve?

A

Shift dose response curves to the right

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4
Q

Increasing amounts of this progressively inhibits the agonist

A

Competitive antagonism

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5
Q

Non-competitive antagonism

A

Even high concentrations of the agonist can not cause the agonist effect

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6
Q

Inverse agonist drugs (6)

A

LMNCPP

Loratadine, metoprolol, naloxone, cetirizine, prazosin, propanolol

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7
Q

This type of agonists causes less response than the agonist even at supramaximal doses

A

Partial agonist

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8
Q

Inverse agonist

A

compete for the same site as the agonist but produce the opposite effect; were categorized as agonists

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9
Q

Does the number of receptors stay the same?

A

No! It can increase or decrease depending on age, disease state, comorbidity, drug therapy, etc.

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10
Q

What are 4 examples of the number of receptors changing?

A

-Tachyphylaxis
-Albuterol treatment for asthma (down regulation of receptors due to repetition)
-Pheochromocytoma (decreased beta receptors in response to catecholamines)
-Ephedrine

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11
Q

How are receptor types classified?

A

By location!

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12
Q

Receptor locations (3)

A

-Lipid bilayer
-Intracellular proteins
-Circulating proteins

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13
Q

This receptor location is common for anesthesia drugs, opioids, benzos, beta blockers, catecholamines and NMBD (B-BACON)

A

Lipid bilayer

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14
Q

This receptor location is common for insulin, steroids and milrinone (SIM)

A

intracellular proteins

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15
Q

This receptor location is common for anticoagulants to bind to

A

circulating proteins

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16
Q

What the body does to the drug

A

pharmacokinetics (ADME)

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17
Q

What type of drugs bind primarily to albumin?

A

acidic drugs

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18
Q

What do alkalotic drugs primarily bind to?

A

Alpha 1-acid glycoprotein

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19
Q

What do you call it when only “free” (unbound) drugs can cross cell membranes?

A

distribution

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20
Q

What do you call it when only a free drug can determine concentration available to receptor?

A

Potency

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21
Q

What can cause decreased plasma proteins?

A

age, hepatic disease, renal failure, pregnancy

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22
Q

Drugs that are plasma protein bound ____% or greater can be impacted by abnormal plasma protein concentration

A

90

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23
Q

If a normal free fraction of a drug is 2% and we lose 50% of proteins, then the free fraction of drugs is __%

A

4%

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24
Q

This drug is highly bound to plasma proteins and has a small volume of distribution

A

warfarin

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25
Q

These two drugs have poor protein binding and they are lipophilic which causes them to have a big volume of distribution

A

thiopental, diazepam

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26
Q

What does metabolism convert?

A

Converts active, lipid soluble drugs into water soluble things (and the metabolites are usually inactive)

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27
Q

Examples of drugs that have active metabolites

A

Diazepam, propanolol, morphine (2 active) and prodrugs such as codeine

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28
Q

How are drugs metabolized in plasma?

A

Hoffman elimination and ester hydrolysis

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29
Q

How are drugs metabolized in the liver?

A

Hepatic microsomal enzymes

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30
Q

What does phase I metabolism pathway do?

A

It increases polarity and prepares for phase II reactions

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31
Q

This is where you lose electrons

A

oxidation

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32
Q

What catalyzes oxidation?

A

CYP450

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33
Q

This process removes oxygen or adds hydrogen molecules

A

reduction

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34
Q

What does phase II metabolism do?

A

Covalently link with a highly polar molecule to become water soluble; conjugation

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35
Q

This phase and cytochrome metabolizes >50% of drugs (opiods, benzos, LA, immunosuppressants, antihistamines)

A

CYP450 Phase I

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36
Q

What does induction to an enzyme do?
Example?

A

Increases the amount of an enzyme

Phenobarbital induces enzymes which increases the metabolism of drugs.

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37
Q

What does inhibition to an enzyme do?
Example?

A

Decreases the activity of enzyme

Grapefruit juice increases the concentration of drugs/toxicity levels

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38
Q

For most anesthetic drugs clearance is ____

A

constant (first order kinetics)

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39
Q

Elimination half time

A

time necessary to eliminate 50% of the drug from plasma after bolus dose

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40
Q

Context sensitive half time

A

Time to a 50% decrease after infusion discontinued

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41
Q

Context sensitive half time ______ the longer the infusion increases due to the accumulation in peripheral tissues

A

increases

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42
Q

Are barbs weak acids or bases?

A

acids

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43
Q

LA and opiods are ____ bases

A

weak

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44
Q

Acids are ionized in an ____ pH

A

alkaline

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45
Q

Bases are ionized in an ___ pH

A

acidic

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46
Q

When the pH and PK are identical……

A

50% of the drug is ionized and 50% of the drug is non ionized

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47
Q

pH < PK

A

Protonated;

Acids unionized
Bases ionized

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48
Q

pH > PK

A

Unprotonated

Acids ionized
Bases unionized

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49
Q

How to write ionization for an acid

A

PK after PH

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50
Q

How to write ionization for a weak base

A

PK before PH

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51
Q

What is the time to drug effect (relative potency)?

A

The lag time between administration (plasma concentration) and effect

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52
Q

Therapeutic index

A

Ratio between LD50/ED50

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53
Q

Enantiomers

A

chemically identical, mirror images, can not be superimposed

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54
Q

Name for an enantiomer that has rotation of light in solution to the right

A

Dextrorotatory

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55
Q

Name for an enantiomer that has rotation of light in solution to the left

A

Levorotatory

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56
Q

What fraction of drugs are racemic

A

1/3

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57
Q

Xoponex is an enantiomer of

A

albuterol

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58
Q

Cisatracurium, the isomer of atracurium, lacks ____ effects

A

histamine effects

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59
Q

This induces calm or sleep

A

Sedatives

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60
Q

Hypnotics

A

induces hypnosis

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61
Q

How does sleep share similarities with anesthesia?

A

It inhibits the thalamic and mid brain RAS and reversibly inhibits CNS

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62
Q

These two things relate to EEG activity

A

CBF and CMRO2

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63
Q

With hypontic drugs, the BIS change correlated with movement. Is this the same for a high dose narcotic?

A

No, with a high dose narcotic there is less correlation between BIS and movement

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64
Q

BIS studies showed that no patient with BIS ____ was conscious

A

<58

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65
Q

What is the suppression ratio on a BIS?

A

It tells you how much of the time the BIS has been zero. Your suppression ratio would never have a number

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66
Q

BIS #0

A

No brain wave activity, brain dead

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67
Q

BIS #100

A

Awake and alert

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68
Q

BIS #40-60

A

Ideal number for no recall

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69
Q

These synergistic drugs lower BIS

A

hypnotics, volatiles, NMBD, opiods

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70
Q

These drugs can increase BIS numbers and confuse picture even though patient is perfectly amnestic

A

Ketamine and epinephrine (sympathomimetics)

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71
Q

Benzos do 5 things:

A

(AAA-SS)

  1. Anxiolytics
  2. Anterograde amnesia
  3. anticonvulsant
  4. Sedation
  5. Spinal cord mediated skeletal muscle relaxation
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72
Q

What is the only thing that can cause retrograde amnesia?

A

ECT

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73
Q

With benzos, anterograde amnesia lasts ____ than sedative effects

A

longer

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74
Q

Why have benzos replaced barbiturates?

A

Barbs have more complications with tolerance, more side effects, and they don’t induce enzymes to be metabolized as quickly

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75
Q

Do benzos induce hepatic microsomal enzymes like barbs?

A

No

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76
Q

Which benzo is used in periop due to its prompt recovery?

A

Versed! Quick on and quick off.

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77
Q

Why are diazepam and lorazepam more attractive for sedation post op?

A

They have a much greater 1/2 time than versed

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78
Q

What is the principal inhibitor neurotransmitter in CNS?

A

GABA

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79
Q

This causes hyper polarization of post synaptic membranes and enhanced opening of Cl- channels

A

GABA

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80
Q

GABA alpha 1 subunit properties

A

sedative, amnestic, anticonvulsant

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81
Q

Most abundant GABA subunit

A

alpha1

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82
Q

GABA alpha 2 subunit properties

A

anxiolytics, skeletal muscle relaxation

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83
Q

All benzos are _____ lipid soluble and _____ protein bound

A

highly, highly

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84
Q

Do benzos cross BBB?

A

Yes

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85
Q

Which benzo does not produce an isoelectric state>

A

Versed; it has a ceiling

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86
Q

What things are synergistic with benzos?

A

Alcohol, injected anesthetics, opiods, alpha 2 agonists, inhaled anesthetics, etomidate

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87
Q

What is the purpose of the imidazole ring in versed

A

Stabilizes the structure and allows for rapid metabolism

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88
Q

This benzo is 2-3x as potent as valium

A

versed (midazolam)

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89
Q

Which benzo has a greater affinity for its receptor, valium or versed?

A

versed

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90
Q

With versed, which effect lasts longer, amnesia or sedation?

A

amnesia > sedation

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91
Q

Versed is water soluble, what does this mean for the formulation?

A

it does not need a solvent added to it! That’s why it does not sting as bad

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92
Q

Explain ring theory versed

A

The ring opening makes it inactive and shutting makes it active!

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93
Q

<3.5 pH the versed ring is ____ which means it is ____ soluble and ______ (active or inactive?)

A

open, water, protonated / inactive

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94
Q

> 4.0 pH the versed ring is ____ which means it is ____ soluble and ______ (active or inactive?)

A

closed, lipid, active/unprotonated

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95
Q

Versed onset

A

1-2 minutes

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96
Q

Versed plasma binding

A

96-98%; extensively bound

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97
Q

Versed peak effect time

A

5 minutes

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98
Q

Why does versed have a relatively short duration?

A

lipid solubility

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99
Q

Versed E 1/2 time

A

2 hours

50% of it will be gone from plasma in 2 hours! Doubled in the elderly.

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100
Q

Versed VD

A

1-1.5L/kg (LARGE)

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101
Q

Why does versed have a larger VD in morbidly obese patients?

A

It is lipid soluble and has more fat it can go into

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102
Q

What enzyme metabolizes versed?

A

CYP3A4

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103
Q

Does versed have an active metabolite?

A

Yes! 1-hydroxymidazolam

This has 1/2 the activity of the parent

104
Q

Drugs that cause inhibition of P450 enzymes and decreased BZD metabolism

A

Fentanyl
Antifungals
CCB
Erythromycin
Tagamet (Cimetidine)

(FACET)

105
Q

Versed has a clearance that is ___ times faster than lorazepam and ____ times faster than diazepam

106
Q

How does versed impact CMRO2 and CBF?

A

The more I give, the more decreased they get - dose related

107
Q

How does versed impact the vasomotor response to CO2?

A

Versed preserves this ability

108
Q

What is the vasomotor response to CO2?

A

When CO2 goes up, it dilates

When CO2 goes down, it vasoconstricts

109
Q

How does versed impact ICP?

A

it doesn’t! Good for induction with neuro pathology

110
Q

How effective is versed as an anticonvulsant?

A

It is a potent anticonvulsant (even in status!)

111
Q

3 pulmonary impacts of Versed

A

-Dose dependent decrease in ventilation (esp with COPD)
-Depresses swallowing reflex
-Decreases upper airway activity

AKA we increase pt risk for aspiration!!!!

112
Q

How does versed impact the BP/HR response to intubation?

A

It does NOT inhibit it; HR and BP will still spike during intubation if you only give versed

113
Q

Sedation dosing VERSED in kids

A

0.25-0.5 mg/kg oral

114
Q

VERSED in kids peak effect time

A

20-30 minutes

115
Q

Sedation dosing VERSED in adults

116
Q

VERSED in adults peak effect time

117
Q

INDUCTION dose VERSED

A

0.1-0.2 mg/kg IV over 30-60 seconds

118
Q

Why do we precede versed induction with an opiod?

A

It picks up the speed of induction

119
Q

If I want to precede my versed induction with fentanyl, how much will I give?

A

Fentanyl 50-100 mcg

120
Q

What drug do you experience emergent excitement with?

121
Q

POST OP SEDATION dose of VERSED

A

1-7 mg/hr IV

122
Q

Issue with versed for post op sedation?

A

-Markedly delayed awakening due to active metabolite accumulating.
-Immune/T cell effects so issues with healing if you leave them on a drip for too long

123
Q

Valium has a ____ duration of action in comparison to midazolam

124
Q

Is valium lipid soluble?

A

Yes, all benzos are highly lipid soluble

125
Q

Is valium soluble in water?

A

NO! Have to add a propylene glycol to it causing painful injection

126
Q

Valium onset

A

1-5 minutes

127
Q

Valium E 1/2 time
Why is it so long?

A

20-40 hours
It is extensively protein bound

128
Q

Compare the dissociation from GABA a in lorazepam vs. valium

A

Valium dissociates from GABA faster than lorazepam. So it has a shorter duration of action but a longer elimination half time. It is around longer, but not on the receptor for as long.

129
Q

What enzyme metabolizes valium?

130
Q

Valium active metabolites and their issues

A

Desmethyldiazepam and oxazepam
They are nearly as potent as diazepam and we see a return of drowsiness 6-8 hours later

131
Q

Dose for valium as an anticonvulsant

A

0.1 mg/kg IV

132
Q

Can valium produce an isoelectric EEG?

133
Q

Pulmonary effects of valium

A

Minimal effects on ventilation!
-Slight vT decrease
-After 0.2 mg/kg IV we see an increase in PaCO2

134
Q

Why was valium great for cardiac surgery induction?

A

It minimally decreases BP, CO and SVR **even with induction doses!
Unchanged even with addition of nitrous.

135
Q

Valium effects on the neuromuscular system

A

Causes spinal cord inhibition which is relaxation at the spinal cord level; does NOT cause NMJ effects so NO paralysis

136
Q

INDUCTION dose VALIUM

A

0.5-1 mg/kg IV

137
Q

In which patient populations would we decrease the valium induction dose by 25-50%

A

Elderly, liver disease, presence of opiods

138
Q

Ativan resembles _____ however, Ativan has an ____ Chloride atom

A

Oxazepam (serax), extra chloride atom

139
Q

Compared to versed and valium, how potent is Ativan as a sedative and amnestic?

A

more potent!
We can give a smaller dose and get a greater effect.

140
Q

Is Ativan soluble in water? What does this mean for its formulation?

A

NO! It requires a solvent such as polyethylene glycol and burns when given IV

141
Q

Why does Ativan have a slower onset of action compared to valium and versed?

A

It is not quite as lipid soluble; slower entry into CNS

142
Q

Why does Ativan have a slower metabolic clearance compared to valium and versed?

A

It has lower lipid solubility; gets across bilayer and to effector site slower and comes back across lipid bilayer into blood slower as well

143
Q

Ativan peak effect for IV dose

A

20-30 minutes

**4-6x longer than versed

144
Q

E 1/2 time Ativan

145
Q

Does Ativan have active metabolites? why or why not?

A

NO. It is conjugated into inactive metabolites via glucuronidation

146
Q

Why is Ativan a good choice for liver disease patients?

A

It is not entirely dependent upon hepatic enzymes for metabolism! It can directly conjugate itself to be metabolized

147
Q

Ativan dose

148
Q

What type of antagonist is Romazicon?

A

Competitive antagonist with a high affinity for BZD receptor

149
Q

Why do you have to repeat doses of romazicon?

A

The sedative itself outlasts the effect of the romazicon; repeat doses until benzo is out of the system

150
Q

Romazicon dose
Max dose?

A

Initial: 0.2 mg IV; titrated to consciousness.
Repeat: 0.1 mg q1 minute to a total of 1mg total
Give until you get the LOC you want or a man of 1 mg

151
Q

Romazicon can result in reversal within __ minutes

152
Q

What dosage range of romazicon is used to abolish therapeutic dose?

153
Q

Duration of flumazenil

A

30-60 minutes

154
Q

Flumazenil gtt dose

A

0.1-0.4 mg/hr

155
Q

Flumazenil side effects

A

None really, except for reversing chronic anxiety or seizure meds

156
Q

Endogenous histamines

A

basophils and mast cells

157
Q

What does histamine induce?

A

Contraction of smooth muscle in airways
Secretion of acid in stomach
Release of neurotransmitters in the CNS (ACh, Norepi, serotonin)

158
Q

What drugs cause drug induced histamine release?

A

Protamine
Atracurium
Morphine
Mivacurium

159
Q

How to treat drug induced histamine release?

A

H1 and H2 antagonists

160
Q

Effects of histamine on H1 receptor

A

Hyperalgesia and inflammatory pain
Allergic rhino-conjunctivitis symptoms

161
Q

Effects of histamine on H2 receptor

A

Elevates CAMP (B1-like stimulation)
Increases acid/volume production

162
Q

Effects of H1 and H2 receptor activation

A

Hypotension due to nitric oxide release, capillary permeability, flushing and prostacyclin release

163
Q

Histamine receptor antagonists are what type of antagonist?

A

Inverse agonists
competitive, reversible

164
Q

T/F
Histamine receptor antagonists do not prevent the release of histamine but responses of the body to histamine

165
Q

Where are H1 receptors located?

A

Airway smooth muscle, cardiac endothelium and vestibular system

166
Q

H1 receptor antagonists side effects

A

-blurred vision
-URINARY RETENTION
-dry mouth
-DROWSINESS (1st gen)

167
Q

H1 receptor antagonist drugs; 1st gen

A

Benadryl, promethazine (phenagren)

168
Q

H1 receptor antagonist drugs; 2nd gen

A

Cetirizine (Zyrtec) and Loratadine (Claritin)

169
Q

Benadryl dose

A

25-50 mg IV

170
Q

Benadryl E 1/2 time

A

7-12 hours

171
Q

What reflex does Benadryl maybe inhibit?

A

Oculi-emetric reflex

172
Q

Promethazine (phenergan) E 1/2 time

A

9-16 hours

173
Q

Promethazine (phenergan) dose

A

12.5-25 mg IV

174
Q

Promethazine (phenergan) onset

175
Q

Black box warning for Promethazine (phenergan)

A

-Infiltration bad; make sure you have a good IV
-Bronchospasm in kids under 2; fatal

176
Q

What 3 things do H2 receptor antagonists do?

A

Decrease gastric volume, increase stomach pH and decrease hyper secretion of hydrogen ions into gastric fluid

177
Q

What class of drugs are Cimetidine (Tagamet), ranitidine (Zantac) and famotidine (Pepcid)?

A

H2 receptor antagonists

178
Q

What enzyme does cimetidine (Tagamet) inhibit

179
Q

What drugs are metabolized by CYP450

A

-Warfarin
-Phenytoin
-Lidocaine
-TCAs
-Propanolol
-Nifedipine
-Meperidine
-Diazepam

180
Q

What H2 antagonist can cause increased levels of prolactin and impotence in men

A

cimetidine

181
Q

Cimetidine (Tagamet) dose

Renal impairment dose?

A

150-300 mg IV
1/2 dose for renal impairment

182
Q

This H2 antagonist weakly binds to CYP enzymes resulting in very few interactions

A

Ranitidine (Zantac)

183
Q

Ranitidine (Zantac) dose

Renal dose?

A

50 mg diluted to 20 cc over 2 minutes

1/2 dose for renal impairment

184
Q

This H2 antagonist does not interfere at all with CYP enzymes resulting in NO interactions

A

famotidine (Pepcid)

185
Q

Most potent H2 antagonist? with a half life of 2.5-4 hours

186
Q

What electrolyte does Pepcid interfere with?

A

Phosphate absorption; hypophosphatemia

187
Q

Famotidine (Pepcid) dose

Renal dose?

A

20 mg IV

1/2 dose

188
Q

How do PPIs bind to pumps?

A

They irreversibly bind to acid secretion pumps! They only inhibit the currently functioning pumps not the ones that have not been made yet! Our body constantly makes proton pumps that’s why you have to continue the drug

189
Q

Are PPIs better for acute or preemptive use?

A

Preemptive!

190
Q

PPIs have been associated with…

A

Bone fx, SLE, nephritis, C-diff and B12 / mag deficiency

191
Q

PPIs block the enzyme that ____ clopidogrel

192
Q

How does PPIs impact warfarin?

A

They inhibit the metabolism of warfarin; our INR will be high

193
Q

Prilosec (omeprazole) dose

A

40 mg in 100 cc NS over 30 minutes; piggy back not push.

PO must be >3 hours prior

194
Q

Is Prilosec a prodrug or active drug?

195
Q

What % max inhibition will you see with Prilosec?

196
Q

What side effects of omeprazole indicate it crosses the BBB?

A

HA, agitation, confusion

197
Q

Protonix 1/2 time compared to prilosec

A

Protonix has a longer E 1/2 time compared to prilosec

198
Q

It only takes proton pump inhibitors __ hr(s) to decrease gastric volume and raise pH. It takes ___ days to inhibit ALL functioning proton pumps

A

1 hour, 5 days

199
Q

Protonix dose

A

40 mg in 100 mL over 2-15 minutes

200
Q

PPIs are the DOC for these 2 things

A

GERD and gastroduodenal ulcers

201
Q

If we have concerns for aspiration will we give a. H2 antagonist or a PPI?

A

H2 antagonist because they work faster

202
Q

Particulate antacids are ___ or ___ based

A

aluminum or mag

203
Q

Why do we not give particulate antacids?

A

More dangerous to aspirate on the particle

204
Q

Non particulate antacids have what bases?

A

Sodium, carbonate, citrate and bicarbonate

205
Q

What is a non-particulate antacid?

A

Sodium citrate / bicitra

206
Q

This antacid is given to all c section ladies

A

BICITRA; uterus being manipulated makes mom nauseous! This drug decreases risk for aspiration pneumonia! Not the risk for aspiration

207
Q

How long does it take for bicitra to kick in? How long does it take for it to lose effectiveness?

A

immediately kicks in, loses effectiveness in 30-60 minutes

208
Q

Bicitra dose

A

15-30 mL PO

209
Q

Who is considered full stomachs

A

Trauma pt, pregnant ladies 12-16 weeks or greater

210
Q

How do dopamine blockers help with full stomach?

A

They are pro kinetic (stimulate GI motility) and work on getting stuff out of the stomach so there is nothing left to aspirate

211
Q

Dopamine blockers effects on GI system (3)

A

-Increases lower esophageal sphincter tone
-Stimulates peristalsis
-Relaxes pylorus and duodenum

212
Q

What are the three dopamine blockers?
Which one is off market?

A

Reglan, droperiodol and Domperidone

-Domperiodone taken off market due to dysrhythmias and sudden death

213
Q

Do dopamine blockers alter gastric pH?

A

no, they just move things forward so you can not throw up

214
Q

Bad effects of dopamine blockers

A

-Extrapyramidal reactions (crosses BBB easy)
-Orthostatic hypotension
-Some effects on chemoreceptor trigger zone
can not give to pt with dopamine depletion / inhibition (Parkinson’s and Huntingtons)

215
Q

This drug is cleard by the FDA for gastroparesis

A

Reglan (metoclopramide)

216
Q

Side effects of reglan:

A

-Abd cramps (due to squeezing of sphincter and increased propulsion of stomach)
-Muscle spasms
-Sedation or extrapyramidal symptoms (crosses BBB)
-Neuroleptic malignant syndrome
-decreases plasma cholinesterase levels

217
Q

Why does succ last longer when you administer reglan to a patient?

A

Reglan decreases plasma cholinesterase level which slows the metabolism of succ

218
Q

Reglan dose
Timing

A

10-20 mg IV over 3-5 minutes
15-30 min prior to induction

219
Q

Does domperidone cross the BBB?

220
Q

This dopamine blocker is related to haldol

A

Droperidol (inapsine)

221
Q

This dopamine 2 antagonist was developed for schizophrenia and psychosis

A

droperidol (inapsine)

222
Q

Droperidol risk factors / side effects and black box warnings

A

-Extrapyramidal symptoms
-Neuroleptic malignant syndrome
-Avoid other CNS depressants (such as general anesthetics)
-Black box: prolonged QT and torsades with higher doses
-LOTS of serious drug interactions (amio, diuretics, sotalol, CCBS)

223
Q

This drug is more effective than reglan and equally effective to 4mg zofran but not often used due to the crazy side effects

A

droperidol

224
Q

Droperidol dose

A

0.625-1.25 mg IV

225
Q

Where is serotonin released from?

A

chromaffin cells in small intestine

226
Q

What receptor does serotonin hit that stimulates vagal afferents and causes vomiting?

227
Q

Where are serotonin receptors found? Which ones do we care about?

A

EVERYWHERE! we are concerned with the ones in the brain and GI tract

228
Q

Can I use a 5HT3 antagonist for motion sickness?

229
Q

Name the 3 5HT3 antagonists

A

-Zofran
-Granisetron (kytril)
-Dolasetron (Anzemet)

230
Q

This is the first 5-HT3 antagonist

231
Q

How does zofran impact:

-Dopamine, histamine, adrenergic and cholinergic activity?
-CNS
-QT interval

A

It doesn’t
No CNS effects
SLIGHT Prolongation of QT interval

232
Q

Plasma 1/2 life of Zofran

233
Q

Zofran dose

234
Q

We do not know the MOA behind corticosteroid for n/v but we think it has to do with these two things:

A
  1. controlling endorphin release
  2. anti inflammatory, less post op pain, less opiods administered
235
Q

Name the corticosteroid we talked about

A

Decadron (dexmethasone)

236
Q

Decadron has a delay in onset of ___ hours.
What does this mean for you?

A

2 hours

If you have a 6 hour case, give it 4 hours into the operation

If you have a 2 hour case, give it as soon as the case starts

237
Q

Efficacy of decadron persists for ___ hours

238
Q

We usually time decadron 2 hours before the end of a case. What is the exception to this rule?

A

Difficult intubations! We want to prevent airway swelling because swelling will interfere with the patient’s ability to maintain their own airway.. then we would not be able to extubate them

239
Q

Decadron side effects?

A

Hyperglycemia (not a concern with only one dose)
Perineal burning / itching

240
Q

Decadron dose for N/v

241
Q

Decadron dose for airway swelling concerns

242
Q

How does scopolamine work at its receptor?

A

It is a competitive antagonist of ACH

243
Q

Scopolamine peak concentration

A

8-24 hours

244
Q

Apply a scopolamine patch __ hours preop

245
Q

Side effects of scopolamine

A

dilated pupil, drowsiness

246
Q

Scopolamine dose

A

1 patch for 24-72 hours post auricular

247
Q

Scopolamine priming dose?

A

140 mcg then 1.5 mg over next 72 hours

248
Q

How potent is scopolamine at being an antisialagogue?

A

Very! it dries up spit

249
Q

Explain how beta receptor agonists relax the airway

A

-Stimulatory G proteins
-activate cAMP
-This decreases Ca entry
-this decreases contractile protein sensitivity to calcium
-This results in relaxation

250
Q

The side effects of beta agonists are similar to…

A

what catecholamine release causes

251
Q

Beta agonist side effects

A

tremor, tachycardia, transient decrease in arterial oxygenation, hyperglycemia

252
Q

We can see a 15% increase in FEV1 with beta agonists after ___ minutes

A

6 minutes (with 2 puffs)

253
Q

Explain delivery of inhaled SABA

A

Discharge inhaler (2 puffs) while taking a slow, deep breath over 5-6 seconds.
Hold breath at max inspiration for 5-6 seconds

254
Q

Diethyl ether was made from

A

sulfuric acid and etyhl alcohol

255
Q

Anesthesia is a drug induced loss of ____

A

consciousness

256
Q

Most recent anesthethic gas

A

Sevoflurane

EB- Advanced Pharm (3 decks)

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