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
Issue with cyclopropane? Halothane?
C = highly explosive H = Slow onset and can cause hepatitis. Good because it causes bronchodilation
26
Compare speeds of Desflurane, Sevoflurane and Isoflurane
Des = fastest onset and emergence Sevo = in between Isoflurane = slowest onset/emergence of the three
27
Who did much of the research on modern volatiles?
Dr. Egar
28
What causes amnesia?
Stimulation of inhibitory transmission (ACh) or inhibition of stimulatory transmission (GABA)
29
What is the anesthesia triad?
Amnesia, Analgesia and Muscle relaxation
30
What is Neurolept anesthesia?
You "screw up the brain" to induce amnesia. Involves lots of anti-psychotics and minimal muscle relaxants/opioids.
31
What is stage 1 of anesthesia? Each plane?
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
32
What is stage 2 of anesthesia?
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
33
What is stage 3 of anesthesia? Each plane?
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)
34
What is stage 4 of anesthesia?
Stoppage of respiration to death
35
What stages do you extubate at? Why?
1 or 3, 2 has a high incidence rate of laryngospasm, N/V
36
What stage do you intubate at?
Stage 3
37
Per lecture, what common pressor agent has a high incidence of tachyphylaxis?
Ephedrine
38
What is the 1 compartment model?
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
39
What is the 2 compartment model?
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.
40
What drugs are listed as sensitive to first pass metabolism?
Lidocaine, propranolol, demerol, fentanyl, sufentanil, alfentanil
41
What protein do acidic drugs bind to? Basic?
Acid = albumin Base = A1-Acid Glycoprotein
42
Which drugs are generally more inactive, water or lipid soluble?
Water
43
What metabolizes most of our anesthesia drugs?
Liver microsomal enzymes
44
What are the primary functions of phase I reactions? Phase II?
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
45
What is the primary microsomal enzyme? And the most common of that family?
CYP450, and the most common of that subclass is CYP3A4
46
Induction vs inhibition?
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
47
Elimination half-time vs elimination half-life?
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)
48
Context sensitive half time?
This is half-time related to an infusion. Basically, the longer an infusion goes, the longer it takes for its effects to wear off.
49
Does ionized or non-ionized more easily cross barriers?
Non-ionized
50
What is the mental trick to remember how to solve ionization problems?
Weak Acid PK after pH (a for after), weak base pK before pH (b for before)
51
Why would a LA not work for a necrotic limb in regards to pH?
Many LA's are weak bases, if the pH is too low, the LA is likely to ionize and therefore not work
52
Definition of chiral?
A molecule with asymmetric centers
53
What is the term for a right rotation of light? Left?
R = Dextrorotatory L = Levorotatory
54
Why do we give anti-anxiety meds in pre-op?
To reduce catecholamine cascade
55
Sedative vs hypnotic?
S = drug that induces sleep or calm H = Drug that induces hypnosis or sleep
56
In regards to an EEG, is even/odd on the left or right?
Odd = left, Even = right
57
BIS terms: SQI, EMG, EEG and SR?
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
58
Goal BIS range?
40 - 60
59
What are the 5 main effects of BZDs?
Anxiolysis, sedation, anterograde amnesia, anticonvulsant action and spinal-cord mediated skeletal muscle relaxation
60
Alpha 1 vs Alpha 2 in a GABA receptor?
Alpha 1 = sedative, amnestic and anti-convulsant Alpha 2 = anxiolytic and skeletal muscle relaxer
61
What BZD clears the fastest?
Versed
62
What BZD is an aspiration risk?
Versed
63
What BZD can produce an isoelectric baseline?
Valium
64
What BZD is best for a COPD patient?
Valium
65
What BZD is not dependent on hepatic enzymes?
Ativan
66
What BZD is the most potent sedative/amnestic?
Ativan
67
What BZD is the most potent muscle relaxer?
Valium
68
What BZD has the slowest onset of action?
Ativan
69
What BZD does not have active metabolites?
Ativan
70
Relationship of CBF and CRMO to EEG?
Direct correlation, as CBF and CRMO increase, the EEG waveform number should increase
71
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?
Bis less than 58 = unconscious Bis less than 65 for the 5% chance
72
What is important to note about the spinal-cord mediated skeletal muscle relaxation with BZDs?
It is not adequate for surgery, you will still need muscle relaxants or paralyzers. It does NOT potentiate NMBD
73
Why did BZDs replace barbiturates?
Less tolerance, less potential for abuse, fewer and less serious side effects, and do not induce hepatic microsomal enzymes
74
How does a BZD work?
Binds to a GABA receptor, allows Cl to come in, hyperpolarizing the target and making it harder to excite
75
What other drugs/chemicals can bind to GABA sites (*hint* think GABA potentiation)?
Barbiturates, etomidate, propofol and alcohol
76
In general are BZDS highly/poorly protein bound and water/lipid soluble?
Highly protein bound and highly lipid soluble
77
What are the general effects of BZDs on the EEG?
Decreased a-alpha activity, antegrade amnesia, some unable to produce isoelectric state
78
What drugs/chemicals are synergistic with BZDs?
Alcohol, injected anesthetics, opioids, alpha-2 agonists (clonidine, precedex, guanfacine), inhaled anesthetics
79
What is a potential anecdotal concern with BZDs intraop?
Reduced platelet aggregation
80
What is the relationship of the imidazole ring to BZD drug availability in pH changes?
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
81
Which drugs are known to cause inhibition of P-450 enzymes and decrease BZD metabolism?
Cimetidine, erythromycin, CCBs, anti-fungals and fentanyl
82
Dosing range for versed in children and adults for sedation?
C = 0.25-0.5 mg/kg Oral (peak 20 - 30 minutes) A = 1 - 5 mg IV, peak 5 minutes
83
Induction dose of versed?
0.1 - 0.2 mg/kg IV over 30 - 60 seconds given AFTER 50 - 100 mcg of fentanyl
84
Post-op dose for sedation for versed?
1 - 7 mg/hr IV
85
Why is post-op sedation with versed now discouraged?
Markedly delays awakening (active metabolites) and can negatively impact the immune T cells
86
What BZD is not a vesicant?
Versed
87
List the BZDs from shortest to longest E1/2 times
Versed (2 hours) < Ativan (14 hours) < Valium (20 - 40 hours)
88
What is the valium dosage for anti-convulsant actions?
0.1 mg/kg IV
89
At what dose does valium begin to cause hypercapnia (it is still the BZD of choice for COPD patients)
0.2 mg/kg IV, and in general, the ventilatory depression is countered by the stimulation of the surgery
90
Which BZD has the most minimal impact on the CV system?
Valium
91
Induction dose for valium?
0.5 - 1.0 mg/kg IV (decrease by 25 - 50% for elderly)
92
What is the structural difference of Ativan to Serax?
It has an extra Cl atom
93
Dosing range for Ativan?
1 - 4 mg IV
94
What is the metabolism route for flumenazil?
Via hepatic microsomal enzymes in inactive metabolites
95
Dosing guidelines for flumenazil?
0.2 mg IV and titrate to consciousness, repeat by 0.1 mg q1m to 1 mg total
96
Dosing range for flumenazil to reverse sedation and abolish therapeutic dose?
Reverse sedation = 0.3 - 0.6 mg Abolish therapeutic dose = 0.5 - 1 mg
97
What releases endogenous histamine?
Basophils and mast cells
98
Effects of histamine in the body?
Contraction of smooth muscle in the airways, secretion of stomach acid, release of neurotransmitters in the CNS (ACh, norepi, serotonin)
99
What drugs can induce histamine release?
Morphine, mivacurium, protamine and atracurium. If any of these are given you must treat with an H1 and an H2 antagonist
100
What does histamine do to H1 receptors? H2?
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
What are the general effects of H1/H2 receptor activation?
Hypotension, capillary permeability, flushing, prostacyclin release, tachycardia
102
Where are the H1 receptor?
In the vestibular system, airway smooth muscle and cardiac endothelial cells
103
What is an advantage of H1 antagonists?
They have little to no tachyphylaxis
104
H1 antagonist s/e and drug examples?
S/E = blurred vision, urinary retention, dry mouth, drowsiness (1st gen only) Drugs = benadryl, phenergan (these are the 1st gen), zyrtec and claritin
105
What is benadryl given for?
Anti-pruritic, pre treat for allergy for dye and anaphylactic reactions
106
E1/2 time for benadryl?
7 - 12 hours
107
What are some positive effects of Benadryl?
Stimulates ventilation by augmenting the relationship of hypoxic/hyper-carbic drives
108
What is the dosing range for benadryl?
25 - 50 mg IV
109
Primary use for phenergan?
Anti-emetic
110
E1/2 for phenergan?
9 - 16 hours
111
What are the secondary uses for Phenergan?
As a rescue drug for PONV and reduce peripheral pain level (has anti-inflammatory action)j
112
What are the black box warning for Phenergan?
Vesicant and respiratory arrest concerns in children under the age of 2
113
Dose and onset for phenergan?
12.5 - 25 mg IV and 5 minutes
114
How do H2 receptor antagonists work?
Decrease hypersecretion of gastric fluid from the gastric parietal cells, decrease cAMP, decrease gastric volume, increase pH
115
General S/E of H2 receptor antagonists?
Diarrhea, HA, skeletal muscle pain, weakened gastric mucosa (infection concerns for the lung), bradycardia, increase in serum creatinine
116
H2 receptor drug examples?
Cimetidine (tagamet), ranitidine (zantac) Famotidine (pepcid)
117
How is tagamet metabolized?
In the liver via CYP450, cleared in the urine
118
Downside of Tagamet?
Strongly inhibits CYP450 (drugs like warfarin, phenytoin, lidcaine, TCAs, propranolol, nifedipine, Demerol and Valium can last longer)
119
S/E of Tagamet?
Bradycardia, hypotension, increased prolactin, impotence (inhibits dihydrotestosterone from binding)
120
Dosing range for Tagamet?
150 - 300 mg IV (1/2 the dose in renal impairment)
121
How is Zantac metabolized?
In the liver and cleared by the kidneys
122
Relationship of Zantac to CYP450?
Does bind, but more weakly than Tagamet and does not inhibit the enzyme
123
Dosing range for Zantac?
50 mg diluted to 20 cc given over 2 minutes (1/2 the dose in renal impairment)
124
How is Pepcid metabolized?
Hepatic metabolism, renally cleared
125
Relationship of Pepcid to CYP450?
No interference
126
Only H2 antagonist that inhibits CYP450?
Tagamet
127
What drug is indicated to inhibit the oculo-emetic reflex?
Benadryl
128
Most potent H2 antagonist? What is its E1/2 time?
Pepcid, 2.5 - 4 hours (the longest of the H2 blockers)
129
What does Pepcid interfere with?
Phosphate absorption
130
Dosing range for Pepcid?
20 mg IV (1/2 the dose in renal impairment)
131
General trends for PPIs?
Takes 3 - 5 days to fully "work", most effective at controlling gastric acidity and decreasing volume
132
What are side effects are PPI's generally associated with with?
Bone fractures, Lupus, nephritis, C-Diff, vitamin b-12 deficiency, magnesium deficiency
133
What drugs can PPI's negatively affect?
Inhibits warfarin metabolism, and blocks enzyme that activates Plavix
134
PPI drugs
Omeprazole (Prilosec), Pantoprazole (Protonix), Lansoprazole (Prevacid) Dexlansoprazole (Dexilent)
135
How is Omeprazole unique from other PPI's?
It is a prodrug and enteric coated
136
Omeprazole metabolism?
By CYP enzymes, theoretically inhibits other drugs but not in a clinically significant manner
137
Omeprazole dose?
40 mg in 100 CC NS over 30 minutes or PO 3 hours prior to surgery
138
Omeprazole S/E?
HA, Agitation, AMS (it can cross the BBB), ABD pain, N/V, flatulence, small bowel bacterial overgrowth
139
Protonix metabolism?
CYP, no significant drug interactions
140
What H2 antagonist is Protonix just as "fast" as?
Ranitidine. Takes about 1 hour to decrease gastric volume and increase pH
141
Protonix dosing?
40 mg in 100 ml over 2 - 15 minutes
142
Drug of choice for GERD?
PPI
143
Drug of choice for Gastric ulcers?
PPI
144
Drug of choice for GI hemorrhage?
PPI after EGD
145
Drug of choice for NSAID ulcerations (specific drug, not class)?
Omeprazole and DC NSAIDs
146
Drug of choice for Aspiration pneumonitis prevention (take timeframe into account)?
Less than 24 hours = H2 Antagonist Greater than 24 hours = PPI
147
Drug of choice for intermittent s/sx of reflux?
H2 antagonists
148
Difference between particulate and non-particulate antacids?
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
Long term downsides to antacids?
Can delay gastric emptying and acid rebound is a concern
150
Concerns with magnesium, calcium and sodium based antacids?
M = diarrhea and neurologic impairment C = hypercalcemia S = increased Na load = extra strain on the CV system d/t fluid overload
151
Downside of giving an antacid prior to surgery?
It does increase gastric volume
152
Dosing for sodium citrate?
15 - 30 ml, give right before surgery as it wears off in 30 - 60 minutes
153
What drug would you give if the patient had a full stomach?
A dopamine blocker because it increases gastric motility
154
Basic effects of dopamine blockers on gastric motility?
Stimulates gastric motility, antagonizes dopamine receptors.
155
Contraindications to a dopamine receptor blocker?
Pt's with dopamine depletion, extrapyramidal reactions, orthostatic hypotension
155
What drug is FDA cleared for diabetic gastroparesis?
Reglan
155
Dopamine receptor blocker drugs?
Reglan, Domperidone and Droperidol (Inapsine)
156
S/E of Pepcid?
ABD pain, muscle spasms, hypotension, sedation, increased prolactin release, neuroleptic malignant syndrome, decrease plasma cholinesterase levels
157
What drugs need to be given with care if Reglan has been administered?
Sux, ester LA, mivacurium. Because Reglan slows metabolism of them and can extend effects of them.
158
S/Sx of neuroleptic malignant syndrome?
High temp, muscle rigidity, tachycardia, confusion
159
Dosing for Reglan?
10 - 20 mg IV over 3 - 5 minutes 15 - 30 minutes prior to induction
160
Which dopamine receptor blocker does not cross the BBB?
Domperidone
161
What was Droperidol originally prescribed for?
Schizophrenia and psychosis
162
Which dopamine blocker has the highest risk for extrapyramidal s/sx and NMS (neuroleptic malignant syndrome)?
Droperidol
163
What is advantageous about Droperidol?
More effective than Reglan and just as effective as Zofran (plus its cheaper)
164
Black box warning for Droperidol?
QT elongation -> Torsaddes, and has A LOT of drug interactions with medications that can affect the heart
165
Dosing for Droperidol?
0.625 - 1.25 mg IV
166
Describe the process of serotonin release
Released from chromaffin cells of the small intestine -> stimulates Vagal afferents via 5HT3 receptors -> vomiting
167
Highest concentration of 5HT3 receptors?
Brain and GI tract
168
5HT3 antagonists?
Ondansetron (Zofran), Granisetron (Kytril) and Dolasetron (Anzemet)
169
Advantages of Zofran? S/E?
Advantages = no CNS activity, no Dopamine/histamine/adrenergic/cholinergic activity. S/E = HA, diarrhea, QT elongation
170
Dosing for Zofran? Half life?
4 - 8 mg IV, and about 4 hours
171
What is the theory of why Decadron works for N/V?
Inhibition of prostaglandin synthesis and control endorphin release. Because it is an anti-inflammatory it can reduce opioid use = lesser chance of NV
172
Decadron onset?
Takes 2 hours to kick in and lasts for 24 hours
173
S/E of decadron?
Hyperglycemia (minimal if not many doses are given) and perineal burning/itching if given too fast IVP
174
Dosing of Decadron?
Varies, start with 4 - 8 mg, uptitrate if needed
175
Primary effects of Scopolamine patch?
Sedation, Anti sialagogue (fancy speak for dry mouth), reduce motion sickness, mydriasis cycloplegia (pupil dilation)
176
Scopolamine dosing and timing?
Apply 4 hours preop, lasts 24 - 72 hours, gives a 140 mcg priming dose then 1.5 mg over 72 hours.
177
Best site for Scopolamine patch?
Post-auricular, secondary = wrist or back
178
How do broncho dilators work?
Activate cAMP = broncho relaxation, decrease Ca entry and contractile sensitivity to Ca. Reduce inflammation and directly relax smooth muscle
179
How much airway relaxation does a SABA achieve?
15% increase in FEV
180
How much of an inhaled SABA reaches the lungs?
12%
181
How much does an ETT reduce drug delivery if aerosolized into the tube?
by about 50 - 70%
182
Beta agonist S/E?
Tremor, tachycardia, transient decrease in arterial oxygenation, hyperglycemia
183
Inhaled beta agonist drugs?
Albuterol (proventil) and Levo-albuterol (xopenex)
184
Which PPI can cross the BBB?
Omeprazole
185
What would you give to an OB patient with a full stomach going into surgery?
Sodium Citrate (Bicitra)
186
How do dopamine blockers help with full stomach?
Stimulate peristalsis, constrict the esophageal sphincter tone and relax the pylorus/duodenum (lower tract)
187
With these drugs, which one requires the RN to wash their hands after administration?
Scopolamine patch - if you don't, and say rub you eye you could severely dilate it
188
Who made the first anesthesia machine with nitrous and oxygen?
Hewitt
189
Which dentist was an early proponent of ether?
William Morton
190
What 2 people were early experimenters with chloroform? Their professions?
Sir James Simpson and Dr. John Snow, obstetricians
191
Who discovered that chloroform had hepatotoxicity in children?
Guthrie
192
Who discovered that light chloroform created fatal VF in animals?
Levy
193
Who understood early on shorter surgeries were preferable?
Dr. Liston (killed 3 men in one surgery)
194
Who worked at the cleveland clinic and was first to use local infiltration of LA using procaine?
Dr. George Crile
195
Who started using regional blocks and kept strict records of vital signs?
Harvey Cushing
196
What metabolizes Valium?
CYP3A4
197
What receptors are in the lipid bilayer?
Opioids, BZDs, B-blockers, catecholamines and NMBD's
198
What receptors are intracellular?
Insulin, steroids, Milrinone
199
What receptors are circulating proteins?
Anti-coagulants
200
What was organized to explore young deaths with chloroform? It's findings?
The Hyderabad commissions - deaths related to apnea -> hypoxia -> cardiovascular collapse
201
When discovered, what was Isoflurane's advantages over Halothane?
Less N/V, safer and quicker onset than Halothane
202
Who discovered that end-tidal concentration correlated to movement, or MAC?
Dr. Egar
203
What classes of drugs are most common to pre-op?
BZD's, H1/H2 blockers and bronchodilators
204
What drugs are most common to induction?
Etomidate, ketamine, propofol and narcotics
205
What classes of drugs are most common to maintenance of anesthesia?
Inhalation drugs, NMBD's, pressors, blockers
206
What classes of drugs are used in emergence of anesthesia?
NMB reversal, local anesthetics
207
Ventilation vs Oxygenation
V = getting oxygen to the alveoli O = getting the oxygen from the alveoli to the tissues
208
Define pre-emptive analgesia
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
What is an alternative reason that early NO anesthesia was able to induce unconsciousness not related to NO?
Hypoxia, they were breathing pure nitrous oxide, so the LOC could be due to hypoxia
210
Which volatile has a high vapor pressure (evaporates easily) and the highest MAC?
Desflurane
211
What is a potential concern with sevoflurane?
Toxic interactions with the soda lime (mostly disproven)
212
Why is Domperidone not available in the US?
Due to dysrhythmia and sudden death concerns
213
What is advantageous of Domperidone?
Does not cross the BBB (unlike reglan) and no anti-cholinergic activity
214
What sub-unit of GABA is most abundant?
Alpha-1
215
How is versed metabolized?
In the liver by CYP3A4
216
Why is versed useful in patients with CHF?
While it can increase HR and decrease BP, it reduces SVR and maintains the CO.
217
What is unique to versed in being used with intubation?
It does not inhibit the BP/HR response, so lesser chance of hypotension
218
What was the country of origin of Dr. Koller, and who was his colleague?
Viennese and Sigmund Freud
219
What is a disadvantage of desflurane?
Requires a large quantity to achieve anesthesia
220
What technique was used in the 1980s to combat surgical stimulation causing change in vitals despite lack of patient movement?
High dose opioid technique
221
What trend was adopted in the 2000s to reduce opioid use?
The multi-modal approach
222
What changes occur in the case of pheochromocytoma?
Decreased B-receptors due to constant catecholamine release = harder for our pressor drugs to work
223
Which BZD and 1 other drug has a large VD, poor protein binding and lipophilic?
Valium and Thiopental
224
What anti-coagulant is highly protein bound to plasma proteins and a small VD?
Warfarin
225
What molecules prefer to be renally excreted? Hepatically?
Renal = ionized or water soluble Hepatic = non-ionized or lipid soluble
226
When solving PK equations, what type of number do you want?
Negative, the more negative it is, the more likely it will be non-ionized and therefore lipid soluble
227
What kinds of drugs (general class, not specific drugs) does BIS have a high correlation with? Low?
High = hypnotic drugs Low = narcotics
228
Where would you find Alpha-1 receptors? Alpha-2?
1 = cerebral cortex, and thalamus 2 = Hippocampus and amygdala
229
How does valium compare to Ativan in behavior at the GABA site?
Valium dissociates faster from GABA, so it has a shorter duration of action and longer E 1/2 time
230
What is one huge advantage of valium?
Minimal effects on the cardiovascular system, even with induction doses (used to be used frequently in CV cases)
231
What classification of drug action do H1/H2 antagonists fall under?
Inverse agonists
232
What must you avoid with Droperidol?
CNS depressants: barbiturates, opioids, GA
233
What are the 4 major effects of scopolamine?
Sedation, Anti-sialagogue (dry mouth) Mydriasis cycloplegia (dilated pupils) and motion sickness prevention