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Semester 2 TxWes > Pharm Unit 1 > Flashcards

Pharm Unit 1 Flashcards

1
Q

Definition of anesthesia?

A

Lack of feeling or sensation, artificially induced loss of ability to feel pain

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2
Q

What are examples of anesthesia from 4000 to 400 BC?

A

Plants (poppy, coca leaves), acupuncture, ethylene fumes beneath Apollo’s temple, cannabis vapor, carotid compression

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3
Q

What was Hippocrates view of anesthesia?

A

None is needed, it is the job of the patient to stay still so that the Dr may do their work (accommodating the operator)

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4
Q

Who wrote the materia medica? What is it?

A

Dioscordies a surgeon in Nero’s army. It is a pharmacology volume.

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5
Q

Give an example of anesthesia from Roman/Greek times

A

Mandragora and wine, together had a hallucinogenic effect

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6
Q

What was the change in anesthesia in the middle ages?

A

Preference for inhaled agents began, such as a mix of opium, mandrake, hemlock, hyposcyamus (L-isomer of atropine) and water. Reversed with vinegar

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7
Q

What was the first volatile anesthetic? What was its problem? Who discovered it?

A

Diethyl ether, very flammable/explosive. Valerius Cordus

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8
Q

Who invented IV access?

A

Sir Christopher Wren and Robert Boyle

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9
Q

Who discovered NO?

A

Joseph Priestly

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10
Q

Who discovered the basic elements and suggested NO for surgical pain control?

A

Humphry Davy

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11
Q

Which dentist found that NO patients had no recall of pain/injury?

A

Horace Wells

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12
Q

Who started mixing volatiles with air to improve cyanosis?

A

Andrews a Chicago surgeon

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13
Q

Who re-visited ether as an anesthetic combined with Whisky?

A

Crawford Long

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14
Q

First successful demonstration of ether in surgery?

A

1846 in London (via google search, done by Morton)

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15
Q

Who found a way to purify Ether?

A

Dr. Robinson Squibb

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16
Q

Other than flammable, what are disadvantages of ether?

A

Prolonged induction/emergence, high incidence of nausea/vomiting

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17
Q

Who defined pain as actual or potential tissue damage?

A

Sir James Simpson

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18
Q

Who discovered epidemiology?

A

Dr. Snow

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19
Q

Who used cocaine for eye surgery?

A

Dr. Koller

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20
Q

Who did the first regional block with cocaine? Type of block?

A

Dr. Halsted, Mandibular block

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21
Q

Describe the Bier block

A

You elevate the arm, let blood drain. Wrap the arm tightly to squeeze out more blood. Inflate a BP cuff to prevent flow of blood into the arm, then inject lidocaine. The arm should stay numb until either the lidocaine is metabolized, or blood flow is restored

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22
Q

1st CRNA?

A

Sister Mary Bernard

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23
Q

Mother of anesthesia?

A

Alice Magaw

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24
Q

Who opened one of the earliest anesthesia schools?

A

Agatha Hodgins

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25
Q

Issue with cyclopropane? Halothane?

A

C = highly explosive
H = Slow onset and can cause hepatitis. Good because it causes bronchodilation

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26
Q

Compare speeds of Desflurane, Sevoflurane and Isoflurane

A

Des = fastest onset and emergence
Sevo = in between
Isoflurane = slowest onset/emergence of the three

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27
Q

Who did much of the research on modern volatiles?

A

Dr. Egar

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28
Q

What causes amnesia?

A

Stimulation of inhibitory transmission (ACh) or inhibition of stimulatory transmission (GABA)

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29
Q

What is the anesthesia triad?

A

Amnesia, Analgesia and Muscle relaxation

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30
Q

What is Neurolept anesthesia?

A

You “screw up the brain” to induce amnesia. Involves lots of anti-psychotics and minimal muscle relaxants/opioids.

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31
Q

What is stage 1 of anesthesia? Each plane?

A

Stage 1 = beginning of induction to LOC
1st plane = no amnesia/analgesia
2nd plane = amnesia, but only partially analgesic (versed, fentanyl)
3rd plane = complete analgesia/amnesia

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32
Q

What is stage 2 of anesthesia?

A

LOC to onset of automatic breathing. Eyelash reflex disappears, coughing/vomiting/struggling can still occur. This is when we want people to not bother the patient. Laryngospasm a risk as well. You want to get through this stage as fast as possible

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33
Q

What is stage 3 of anesthesia? Each plane?

A

Stage 3 = onset of automatic respiration to respiratory paralysis
1st plane = automatic respiration to cessation of eyeball movements
2nd plane = cessation of eyeball movements to beginning of intercostal muscle paralysis. Tear secretion increases
3rd plane = beginning/completion of intercostal muscle paralysis. Pupils dilate, desired plane prior to muscle relaxants
4th plane = complete intercostal paralysis to diaphragmatic paralysis (apnea)

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34
Q

What is stage 4 of anesthesia?

A

Stoppage of respiration to death

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35
Q

What stages do you extubate at? Why?

A

1 or 3, 2 has a high incidence rate of laryngospasm, N/V

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36
Q

What stage do you intubate at?

A

Stage 3

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37
Q

Per lecture, what common pressor agent has a high incidence of tachyphylaxis?

A

Ephedrine

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38
Q

What is the 1 compartment model?

A

Drug gets injected, goes to heart, circulates through the central circuit and goes to vessel rich groups, then they can leave and go to other places and then be excreted

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39
Q

What is the 2 compartment model?

A

Drugs go into the central compartment and then into the periphery and from there can go other places such as fat or proteins prior to excretion.

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40
Q

What drugs are listed as sensitive to first pass metabolism?

A

Lidocaine, propranolol, demerol, fentanyl, sufentanil, alfentanil

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41
Q

What protein do acidic drugs bind to? Basic?

A

Acid = albumin
Base = A1-Acid Glycoprotein

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42
Q

Which drugs are generally more inactive, water or lipid soluble?

A

Water

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43
Q

What metabolizes most of our anesthesia drugs?

A

Liver microsomal enzymes

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44
Q

What are the primary functions of phase I reactions? Phase II?

A

Phase I = Redox and hydrolysis to increase drugs in polarity to prepare them for phase II

Phase II = Make drugs more water soluble via some form of a conjugation reaction

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45
Q

What is the primary microsomal enzyme? And the most common of that family?

A

CYP450, and the most common of that subclass is CYP3A4

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46
Q

Induction vs inhibition?

A

Induction: enzyme activity is increased leading to a shorter duration of a drug metabolized by the enzyme

Inhibition: enzyme activity is reduced leading to a greater duration

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47
Q

Elimination half-time vs elimination half-life?

A

HT = time to get rid of 50% from the plasma
HL = time to get rid of 50% from the body (tissues for example, hard to measure)

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48
Q

Context sensitive half time?

A

This is half-time related to an infusion. Basically, the longer an infusion goes, the longer it takes for its effects to wear off.

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49
Q

Does ionized or non-ionized more easily cross barriers?

A

Non-ionized

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50
Q

What is the mental trick to remember how to solve ionization problems?

A

Weak Acid PK after pH (a for after), weak base pK before pH (b for before)

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51
Q

Why would a LA not work for a necrotic limb in regards to pH?

A

Many LA’s are weak bases, if the pH is too low, the LA is likely to ionize and therefore not work

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52
Q

Definition of chiral?

A

A molecule with asymmetric centers

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53
Q

What is the term for a right rotation of light? Left?

A

R = Dextrorotatory
L = Levorotatory

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54
Q

Why do we give anti-anxiety meds in pre-op?

A

To reduce catecholamine cascade

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55
Q

Sedative vs hypnotic?

A

S = drug that induces sleep or calm
H = Drug that induces hypnosis or sleep

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56
Q

In regards to an EEG, is even/odd on the left or right?

A

Odd = left, Even = right

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57
Q

BIS terms: SQI, EMG, EEG and SR?

A

SQI: signal quality index, want this maxed
EMG: you want none, meaning no muscle movement
EEG: all brain electrical activity into one waveform
SR: suppression ratio, tells us how often the EEG has been flat

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58
Q

Goal BIS range?

A

40 - 60

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59
Q

What are the 5 main effects of BZDs?

A

Anxiolysis, sedation, anterograde amnesia, anticonvulsant action and spinal-cord mediated skeletal muscle relaxation

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60
Q

Alpha 1 vs Alpha 2 in a GABA receptor?

A

Alpha 1 = sedative, amnestic and anti-convulsant
Alpha 2 = anxiolytic and skeletal muscle relaxer

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61
Q

What BZD clears the fastest?

A

Versed

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62
Q

What BZD is an aspiration risk?

A

Versed

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63
Q

What BZD can produce an isoelectric baseline?

A

Valium

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64
Q

What BZD is best for a COPD patient?

A

Valium

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65
Q

What BZD is not dependent on hepatic enzymes?

A

Ativan

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66
Q

What BZD is the most potent sedative/amnestic?

A

Ativan

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67
Q

What BZD is the most potent muscle relaxer?

A

Valium

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68
Q

What BZD has the slowest onset of action?

A

Ativan

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69
Q

What BZD does not have active metabolites?

A

Ativan

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70
Q

Relationship of CBF and CRMO to EEG?

A

Direct correlation, as CBF and CRMO increase, the EEG waveform number should increase

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71
Q

At what BIS are patients going to be unconscious? At what level do they have less than a 5% chance to return to consciousness within 50 seconds?

A

Bis less than 58 = unconscious
Bis less than 65 for the 5% chance

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72
Q

What is important to note about the spinal-cord mediated skeletal muscle relaxation with BZDs?

A

It is not adequate for surgery, you will still need muscle relaxants or paralyzers. It does NOT potentiate NMBD

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73
Q

Why did BZDs replace barbiturates?

A

Less tolerance, less potential for abuse, fewer and less serious side effects, and do not induce hepatic microsomal enzymes

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74
Q

How does a BZD work?

A

Binds to a GABA receptor, allows Cl to come in, hyperpolarizing the target and making it harder to excite

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75
Q

What other drugs/chemicals can bind to GABA sites (hint think GABA potentiation)?

A

Barbiturates, etomidate, propofol and alcohol

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76
Q

In general are BZDS highly/poorly protein bound and water/lipid soluble?

A

Highly protein bound and highly lipid soluble

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77
Q

What are the general effects of BZDs on the EEG?

A

Decreased a-alpha activity, antegrade amnesia, some unable to produce isoelectric state

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78
Q

What drugs/chemicals are synergistic with BZDs?

A

Alcohol, injected anesthetics, opioids, alpha-2 agonists (clonidine, precedex, guanfacine), inhaled anesthetics

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79
Q

What is a potential anecdotal concern with BZDs intraop?

A

Reduced platelet aggregation

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80
Q

What is the relationship of the imidazole ring to BZD drug availability in pH changes?

A

If the pH is less than 3.5, the ring is open, water soluble and protonated

If the ph is greater than 4.0, the ring is closed, lipid soluble and non-protonated

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81
Q

Which drugs are known to cause inhibition of P-450 enzymes and decrease BZD metabolism?

A

Cimetidine, erythromycin, CCBs, anti-fungals and fentanyl

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82
Q

Dosing range for versed in children and adults for sedation?

A

C = 0.25-0.5 mg/kg Oral (peak 20 - 30 minutes)
A = 1 - 5 mg IV, peak 5 minutes

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83
Q

Induction dose of versed?

A

0.1 - 0.2 mg/kg IV over 30 - 60 seconds given AFTER 50 - 100 mcg of fentanyl

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84
Q

Post-op dose for sedation for versed?

A

1 - 7 mg/hr IV

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85
Q

Why is post-op sedation with versed now discouraged?

A

Markedly delays awakening (active metabolites) and can negatively impact the immune T cells

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86
Q

What BZD is not a vesicant?

A

Versed

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87
Q

List the BZDs from shortest to longest E1/2 times

A

Versed (2 hours) < Ativan (14 hours) < Valium (20 - 40 hours)

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88
Q

What is the valium dosage for anti-convulsant actions?

A

0.1 mg/kg IV

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89
Q

At what dose does valium begin to cause hypercapnia (it is still the BZD of choice for COPD patients)

A

0.2 mg/kg IV, and in general, the ventilatory depression is countered by the stimulation of the surgery

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90
Q

Which BZD has the most minimal impact on the CV system?

A

Valium

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91
Q

Induction dose for valium?

A

0.5 - 1.0 mg/kg IV (decrease by 25 - 50% for elderly)

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92
Q

What is the structural difference of Ativan to Serax?

A

It has an extra Cl atom

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93
Q

Dosing range for Ativan?

A

1 - 4 mg IV

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94
Q

What is the metabolism route for flumenazil?

A

Via hepatic microsomal enzymes in inactive metabolites

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95
Q

Dosing guidelines for flumenazil?

A

0.2 mg IV and titrate to consciousness, repeat by 0.1 mg q1m to 1 mg total

96
Q

Dosing range for flumenazil to reverse sedation and abolish therapeutic dose?

A

Reverse sedation = 0.3 - 0.6 mg
Abolish therapeutic dose = 0.5 - 1 mg

97
Q

What releases endogenous histamine?

A

Basophils and mast cells

98
Q

Effects of histamine in the body?

A

Contraction of smooth muscle in the airways, secretion of stomach acid, release of neurotransmitters in the CNS (ACh, norepi, serotonin)

99
Q

What drugs can induce histamine release?

A

Morphine, mivacurium, protamine and atracurium. If any of these are given you must treat with an H1 and an H2 antagonist

100
Q

What does histamine do to H1 receptors? H2?

A

H1 = “bee sting”, hyperalgesia and inflammatory pain, allergic rhino-conjunctivitis s/sx

H2 = elevates cAMP (beta-1 like stimulation) and increase acid/volume production

101
Q

What are the general effects of H1/H2 receptor activation?

A

Hypotension, capillary permeability, flushing, prostacyclin release, tachycardia

102
Q

Where are the H1 receptor?

A

In the vestibular system, airway smooth muscle and cardiac endothelial cells

103
Q

What is an advantage of H1 antagonists?

A

They have little to no tachyphylaxis

104
Q

H1 antagonist s/e and drug examples?

A

S/E = blurred vision, urinary retention, dry mouth, drowsiness (1st gen only)

Drugs = benadryl, phenergan (these are the 1st gen), zyrtec and claritin

105
Q

What is benadryl given for?

A

Anti-pruritic, pre treat for allergy for dye and anaphylactic reactions

106
Q

E1/2 time for benadryl?

A

7 - 12 hours

107
Q

What are some positive effects of Benadryl?

A

Stimulates ventilation by augmenting the relationship of hypoxic/hyper-carbic drives

108
Q

What is the dosing range for benadryl?

A

25 - 50 mg IV

109
Q

Primary use for phenergan?

A

Anti-emetic

110
Q

E1/2 for phenergan?

A

9 - 16 hours

111
Q

What are the secondary uses for Phenergan?

A

As a rescue drug for PONV and reduce peripheral pain level (has anti-inflammatory action)j

112
Q

What are the black box warning for Phenergan?

A

Vesicant and respiratory arrest concerns in children under the age of 2

113
Q

Dose and onset for phenergan?

A

12.5 - 25 mg IV and 5 minutes

114
Q

How do H2 receptor antagonists work?

A

Decrease hypersecretion of gastric fluid from the gastric parietal cells, decrease cAMP, decrease gastric volume, increase pH

115
Q

General S/E of H2 receptor antagonists?

A

Diarrhea, HA, skeletal muscle pain, weakened gastric mucosa (infection concerns for the lung), bradycardia, increase in serum creatinine

116
Q

H2 receptor drug examples?

A

Cimetidine (tagamet), ranitidine (zantac) Famotidine (pepcid)

117
Q

How is tagamet metabolized?

A

In the liver via CYP450, cleared in the urine

118
Q

Downside of Tagamet?

A

Strongly inhibits CYP450 (drugs like warfarin, phenytoin, lidcaine, TCAs, propranolol, nifedipine, Demerol and Valium can last longer)

119
Q

S/E of Tagamet?

A

Bradycardia, hypotension, increased prolactin, impotence (inhibits dihydrotestosterone from binding)

120
Q

Dosing range for Tagamet?

A

150 - 300 mg IV (1/2 the dose in renal impairment)

121
Q

How is Zantac metabolized?

A

In the liver and cleared by the kidneys

122
Q

Relationship of Zantac to CYP450?

A

Does bind, but more weakly than Tagamet and does not inhibit the enzyme

123
Q

Dosing range for Zantac?

A

50 mg diluted to 20 cc given over 2 minutes (1/2 the dose in renal impairment)

124
Q

How is Pepcid metabolized?

A

Hepatic metabolism, renally cleared

125
Q

Relationship of Pepcid to CYP450?

A

No interference

126
Q

Only H2 antagonist that inhibits CYP450?

A

Tagamet

127
Q

What drug is indicated to inhibit the oculo-emetic reflex?

A

Benadryl

128
Q

Most potent H2 antagonist? What is its E1/2 time?

A

Pepcid, 2.5 - 4 hours (the longest of the H2 blockers)

129
Q

What does Pepcid interfere with?

A

Phosphate absorption

130
Q

Dosing range for Pepcid?

A

20 mg IV (1/2 the dose in renal impairment)

131
Q

General trends for PPIs?

A

Takes 3 - 5 days to fully “work”, most effective at controlling gastric acidity and decreasing volume

132
Q

What are side effects are PPI’s generally associated with with?

A

Bone fractures, Lupus, nephritis, C-Diff, vitamin b-12 deficiency, magnesium deficiency

133
Q

What drugs can PPI’s negatively affect?

A

Inhibits warfarin metabolism, and blocks enzyme that activates Plavix

134
Q

PPI drugs

A

Omeprazole (Prilosec), Pantoprazole (Protonix), Lansoprazole (Prevacid) Dexlansoprazole (Dexilent)

135
Q

How is Omeprazole unique from other PPI’s?

A

It is a prodrug and enteric coated

136
Q

Omeprazole metabolism?

A

By CYP enzymes, theoretically inhibits other drugs but not in a clinically significant manner

137
Q

Omeprazole dose?

A

40 mg in 100 CC NS over 30 minutes or PO 3 hours prior to surgery

138
Q

Omeprazole S/E?

A

HA, Agitation, AMS (it can cross the BBB), ABD pain, N/V, flatulence, small bowel bacterial overgrowth

139
Q

Protonix metabolism?

A

CYP, no significant drug interactions

140
Q

What H2 antagonist is Protonix just as “fast” as?

A

Ranitidine. Takes about 1 hour to decrease gastric volume and increase pH

141
Q

Protonix dosing?

A

40 mg in 100 ml over 2 - 15 minutes

142
Q

Drug of choice for GERD?

A

PPI

143
Q

Drug of choice for Gastric ulcers?

A

PPI

144
Q

Drug of choice for GI hemorrhage?

A

PPI after EGD

145
Q

Drug of choice for NSAID ulcerations (specific drug, not class)?

A

Omeprazole and DC NSAIDs

146
Q

Drug of choice for Aspiration pneumonitis prevention (take timeframe into account)?

A

Less than 24 hours = H2 Antagonist
Greater than 24 hours = PPI

147
Q

Drug of choice for intermittent s/sx of reflux?

A

H2 antagonists

148
Q

Difference between particulate and non-particulate antacids?

A

P = aluminum and magnesium based, and its aspiration is just as bad as an acidic aspiration (don’t reduce volume and increase pH enough especially relative to the NP antacids)

NP = sodium/carbonate/citrate/bicarbonate base, neutralizes acid

149
Q

Long term downsides to antacids?

A

Can delay gastric emptying and acid rebound is a concern

150
Q

Concerns with magnesium, calcium and sodium based antacids?

A

M = diarrhea and neurologic impairment
C = hypercalcemia
S = increased Na load = extra strain on the CV system d/t fluid overload

151
Q

Downside of giving an antacid prior to surgery?

A

It does increase gastric volume

152
Q

Dosing for sodium citrate?

A

15 - 30 ml, give right before surgery as it wears off in 30 - 60 minutes

153
Q

What drug would you give if the patient had a full stomach?

A

A dopamine blocker because it increases gastric motility

154
Q

Basic effects of dopamine blockers on gastric motility?

A

Stimulates gastric motility, antagonizes dopamine receptors.

155
Q

Contraindications to a dopamine receptor blocker?

A

Pt’s with dopamine depletion, extrapyramidal reactions, orthostatic hypotension

155
Q

What drug is FDA cleared for diabetic gastroparesis?

A

Reglan

155
Q

Dopamine receptor blocker drugs?

A

Reglan, Domperidone and Droperidol (Inapsine)

156
Q

S/E of Pepcid?

A

ABD pain, muscle spasms, hypotension, sedation, increased prolactin release, neuroleptic malignant syndrome, decrease plasma cholinesterase levels

157
Q

What drugs need to be given with care if Reglan has been administered?

A

Sux, ester LA, mivacurium. Because Reglan slows metabolism of them and can extend effects of them.

158
Q

S/Sx of neuroleptic malignant syndrome?

A

High temp, muscle rigidity, tachycardia, confusion

159
Q

Dosing for Reglan?

A

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

160
Q

Which dopamine receptor blocker does not cross the BBB?

A

Domperidone

161
Q

What was Droperidol originally prescribed for?

A

Schizophrenia and psychosis

162
Q

Which dopamine blocker has the highest risk for extrapyramidal s/sx and NMS (neuroleptic malignant syndrome)?

A

Droperidol

163
Q

What is advantageous about Droperidol?

A

More effective than Reglan and just as effective as Zofran (plus its cheaper)

164
Q

Black box warning for Droperidol?

A

QT elongation -> Torsaddes, and has A LOT of drug interactions with medications that can affect the heart

165
Q

Dosing for Droperidol?

A

0.625 - 1.25 mg IV

166
Q

Describe the process of serotonin release

A

Released from chromaffin cells of the small intestine -> stimulates Vagal afferents via 5HT3 receptors -> vomiting

167
Q

Highest concentration of 5HT3 receptors?

A

Brain and GI tract

168
Q

5HT3 antagonists?

A

Ondansetron (Zofran), Granisetron (Kytril) and Dolasetron (Anzemet)

169
Q

Advantages of Zofran? S/E?

A

Advantages = no CNS activity, no Dopamine/histamine/adrenergic/cholinergic activity.

S/E = HA, diarrhea, QT elongation

170
Q

Dosing for Zofran? Half life?

A

4 - 8 mg IV, and about 4 hours

171
Q

What is the theory of why Decadron works for N/V?

A

Inhibition of prostaglandin synthesis and control endorphin release. Because it is an anti-inflammatory it can reduce opioid use = lesser chance of NV

172
Q

Decadron onset?

A

Takes 2 hours to kick in and lasts for 24 hours

173
Q

S/E of decadron?

A

Hyperglycemia (minimal if not many doses are given) and perineal burning/itching if given too fast IVP

174
Q

Dosing of Decadron?

A

Varies, start with 4 - 8 mg, uptitrate if needed

175
Q

Primary effects of Scopolamine patch?

A

Sedation, Anti sialagogue (fancy speak for dry mouth), reduce motion sickness, mydriasis cycloplegia (pupil dilation)

176
Q

Scopolamine dosing and timing?

A

Apply 4 hours preop, lasts 24 - 72 hours, gives a 140 mcg priming dose then 1.5 mg over 72 hours.

177
Q

Best site for Scopolamine patch?

A

Post-auricular, secondary = wrist or back

178
Q

How do broncho dilators work?

A

Activate cAMP = broncho relaxation, decrease Ca entry and contractile sensitivity to Ca. Reduce inflammation and directly relax smooth muscle

179
Q

How much airway relaxation does a SABA achieve?

A

15% increase in FEV

180
Q

How much of an inhaled SABA reaches the lungs?

A

12%

181
Q

How much does an ETT reduce drug delivery if aerosolized into the tube?

A

by about 50 - 70%

182
Q

Beta agonist S/E?

A

Tremor, tachycardia, transient decrease in arterial oxygenation, hyperglycemia

183
Q

Inhaled beta agonist drugs?

A

Albuterol (proventil) and Levo-albuterol (xopenex)

184
Q

Which PPI can cross the BBB?

A

Omeprazole

185
Q

What would you give to an OB patient with a full stomach going into surgery?

A

Sodium Citrate (Bicitra)

186
Q

How do dopamine blockers help with full stomach?

A

Stimulate peristalsis, constrict the esophageal sphincter tone and relax the pylorus/duodenum (lower tract)

187
Q

With these drugs, which one requires the RN to wash their hands after administration?

A

Scopolamine patch - if you don’t, and say rub you eye you could severely dilate it

188
Q

Who made the first anesthesia machine with nitrous and oxygen?

A

Hewitt

189
Q

Which dentist was an early proponent of ether?

A

William Morton

190
Q

What 2 people were early experimenters with chloroform? Their professions?

A

Sir James Simpson and Dr. John Snow, obstetricians

191
Q

Who discovered that chloroform had hepatotoxicity in children?

A

Guthrie

192
Q

Who discovered that light chloroform created fatal VF in animals?

A

Levy

193
Q

Who understood early on shorter surgeries were preferable?

A

Dr. Liston (killed 3 men in one surgery)

194
Q

Who worked at the cleveland clinic and was first to use local infiltration of LA using procaine?

A

Dr. George Crile

195
Q

Who started using regional blocks and kept strict records of vital signs?

A

Harvey Cushing

196
Q

What metabolizes Valium?

A

CYP3A4

197
Q

What receptors are in the lipid bilayer?

A

Opioids, BZDs, B-blockers, catecholamines and NMBD’s

198
Q

What receptors are intracellular?

A

Insulin, steroids, Milrinone

199
Q

What receptors are circulating proteins?

A

Anti-coagulants

200
Q

What was organized to explore young deaths with chloroform? It’s findings?

A

The Hyderabad commissions - deaths related to apnea -> hypoxia -> cardiovascular collapse

201
Q

When discovered, what was Isoflurane’s advantages over Halothane?

A

Less N/V, safer and quicker onset than Halothane

202
Q

Who discovered that end-tidal concentration correlated to movement, or MAC?

A

Dr. Egar

203
Q

What classes of drugs are most common to pre-op?

A

BZD’s, H1/H2 blockers and bronchodilators

204
Q

What drugs are most common to induction?

A

Etomidate, ketamine, propofol and narcotics

205
Q

What classes of drugs are most common to maintenance of anesthesia?

A

Inhalation drugs, NMBD’s, pressors, blockers

206
Q

What classes of drugs are used in emergence of anesthesia?

A

NMB reversal, local anesthetics

207
Q

Ventilation vs Oxygenation

A

V = getting oxygen to the alveoli
O = getting the oxygen from the alveoli to the tissues

208
Q

Define pre-emptive analgesia

A

The idea that the longer you can prevent the brain from recognizing pain, the lesser the sensation of pain will be when it is eventually recognized

209
Q

What is an alternative reason that early NO anesthesia was able to induce unconsciousness not related to NO?

A

Hypoxia, they were breathing pure nitrous oxide, so the LOC could be due to hypoxia

210
Q

Which volatile has a high vapor pressure (evaporates easily) and the highest MAC?

A

Desflurane

211
Q

What is a potential concern with sevoflurane?

A

Toxic interactions with the soda lime (mostly disproven)

212
Q

Why is Domperidone not available in the US?

A

Due to dysrhythmia and sudden death concerns

213
Q

What is advantageous of Domperidone?

A

Does not cross the BBB (unlike reglan) and no anti-cholinergic activity

214
Q

What sub-unit of GABA is most abundant?

A

Alpha-1

215
Q

How is versed metabolized?

A

In the liver by CYP3A4

216
Q

Why is versed useful in patients with CHF?

A

While it can increase HR and decrease BP, it reduces SVR and maintains the CO.

217
Q

What is unique to versed in being used with intubation?

A

It does not inhibit the BP/HR response, so lesser chance of hypotension

218
Q

What was the country of origin of Dr. Koller, and who was his colleague?

A

Viennese and Sigmund Freud

219
Q

What is a disadvantage of desflurane?

A

Requires a large quantity to achieve anesthesia

220
Q

What technique was used in the 1980s to combat surgical stimulation causing change in vitals despite lack of patient movement?

A

High dose opioid technique

221
Q

What trend was adopted in the 2000s to reduce opioid use?

A

The multi-modal approach

222
Q

What changes occur in the case of pheochromocytoma?

A

Decreased B-receptors due to constant catecholamine release = harder for our pressor drugs to work

223
Q

Which BZD and 1 other drug has a large VD, poor protein binding and lipophilic?

A

Valium and Thiopental

224
Q

What anti-coagulant is highly protein bound to plasma proteins and a small VD?

A

Warfarin

225
Q

What molecules prefer to be renally excreted? Hepatically?

A

Renal = ionized or water soluble
Hepatic = non-ionized or lipid soluble

226
Q

When solving PK equations, what type of number do you want?

A

Negative, the more negative it is, the more likely it will be non-ionized and therefore lipid soluble

227
Q

What kinds of drugs (general class, not specific drugs) does BIS have a high correlation with? Low?

A

High = hypnotic drugs
Low = narcotics

228
Q

Where would you find Alpha-1 receptors? Alpha-2?

A

1 = cerebral cortex, and thalamus
2 = Hippocampus and amygdala

229
Q

How does valium compare to Ativan in behavior at the GABA site?

A

Valium dissociates faster from GABA, so it has a shorter duration of action and longer E 1/2 time

230
Q

What is one huge advantage of valium?

A

Minimal effects on the cardiovascular system, even with induction doses (used to be used frequently in CV cases)

231
Q

What classification of drug action do H1/H2 antagonists fall under?

A

Inverse agonists

232
Q

What must you avoid with Droperidol?

A

CNS depressants: barbiturates, opioids, GA

233
Q

What are the 4 major effects of scopolamine?

A

Sedation, Anti-sialagogue (dry mouth) Mydriasis cycloplegia (dilated pupils) and motion sickness prevention

Semester 2 TxWes (16 decks)

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