Exam 1 Kane Flashcards
(360 cards)
1
Q
A drug induced loss of consciousness during which pts are not arousable, even by painful stimulation.
A
General Anesthesia
2
Q
A medication that includes more than one enantiomer
A
racemic
3
Q
Agents with chiral molecules that are mirror images of each other are known as
A
enantiomers
4
Q
An agent that activates a specific molecule in a biologic system
A
Agonist
5
Q
Half-life is known as the amt of time to clear ½ of drug from the
A
body
6
Q
Describe Minimal Sedation
A
anxiolysis; normal response to verbal commands, airway unaffected, ventilation unaffected, cardiac unaffected
7
Q
Describe Moderate Sedation
A
Drug-induced depression of consciousness but respond to tactile stimulation, no assistance needed for airway, adequate ventilation, cardiac usually maintained
8
Q
Describe Deep Sedation
A
Stimulation after repeated verbal/touch, Independent ventilation may be impaired; assistance for airway may be required, cardiac usually maintained,
9
Q
Describe allodynia
A
Due to a Stimulus that does not normally cause pain
10
Q
The term that describes Increased pain perception from a stimulus that normally provokes pain
A
Hyperalgesia
11
Q
Increased transduction/transmission of nociception; the process that causes hyperalgesia or allodynia
A
sensitization
12
Q
Pain caused by a lesion or disease of somatosensory nervous system ; Characterized by reduced sensory and nociceptive thresholds
A
Neuropathic Pain
13
Q
Pain transmitted to brain through spinal or cranial nerves
A
Somatic Pain
14
Q
Pain transmitted to brain through autonomic nerves (internal organs)
A
visceral pain
15
Q
Pain in the distribution of a nerve or group of nerves
A
neuralgia pain
16
Q
An agent that activates/inhibits the action of a specific molecule but doesn’t form a permanent bond; other agents may also affect the same site
A
competitive
17
Q
Competitive or noncompetitive agent that activates or inhibits the action of a neurotransmitter but does not function at the binding site
A
Indirect agent
18
Q
Two agents administered at the same time who potentiate each other 1+1=3
A
Synergistic
19
Q
Agents that activates a specific molecule but does not act at the SAME binding site as the neurotransmitter in question
A
Allosteric
20
Q
Acquired hyporeactivity to an agent
A
Tolerance
21
Q
An agent that activates or inhibits a specific molecule and forms a strong or permanent bond so that the other agents may not affect the same site
A
Non-competitive
22
Q
Competitive or non-competitive agent that activates or inhibits the action of a molecule at the same site of action
A
Direct agent
23
Q
Acquire hyporeactivity to an agent that occurs very rapidly
A
Tachyphylaxis
24
Q
Two agents administered at the same time where the total response in the same as the response of one added to the other: 1+1=2
A
Additive
25
An agent that activates or inhibits an action but does not have a high affinity or efficacy for the desired effect
Partial
26
That action of specific molecules are inhibited or blocked by
Antagonist
27
The amount of drug totally cleared from the plasma over time and expressed in L/min
Clearance
28
The dose required to produce a therapeutic response is called
Potency
29
The inability to recall past experiences
Amnesia
30
The maximum therapeutic effect of a drug is known as
Efficacy
31
Which type of pain is described as “unpleaseant sensory and emotional experiences with actual or potential tissue damage” ?
both acute and chronic pain
32
Which type of pain is said to exist BEYOND the healing process
Chronic pain
33
Therapeutic index
Ratio between LD50/ED50 denoting the relative safety of the medication. The higher the ratio the safer the drug
34
Recall
Conscious memory
35
Chirality
subset of stereochemistry that has a center or centers of 3 dimensional asymmetry
36
Stereochemistry
the study of how molecules are structured in three dimensions
37
Pharmacodynamics
Study of the intrinsic sensitivity or responsiveness of the body to a drug and mechanisms by which theses effects occur.
38
Context-sensitive half-time
1. The time required for blood or plasma concentrations of a drug to decrease by 50% after discontinuation of drug administration. Ex: Continuous fentanyl infusion causing half-life to build up over time.
39
First-order processes
Processes where the rate of change varies over time. Processes that occur at a rate proportional to the amount.
40
Zero-order processes
Processes where the rate of change is constant
41
Vessel rich group
Tissues that receive the bulk of arterial blood flow
42
Pharmacokinetics
The quantitative study of the absorption, distribution, metabolism and excretion of injected and inhaled drugs and their metabolites
43
Inverse agonists
Bind at the same site of the agonist but produce the opposite effect of the agonist. Turn off constitutive activity of the receptor
44
Regional Anesthesia
Regional Anesthesia- interrupts sensory nerve conduction of a particular region of the body ( examples include: peripheral blocks, spinals, epidurals), does NOT change level of consciousness ( unless you sedate as well) , can still use airway
45
Dioscorides 40-90 AD (surgeon in NERO’s army)
Materia Medica; Mandragora and wine (harry potter thing) – hallucinogenic, human shaped, magical
46
What is Ether the Greek word for?
Ignite
47
Sir Christopher Wren and Robert Boyle (1650s)
Utilized a goose quill as an IV to give a dog alcohol, probably the first sense of pharmacokinetics
48
Joseph Priestly 1773
Discovers oxygen and nitrous oxide
49
Humphry Davy 1800
Discovered potassium, sodium, calcium, magnesium and suggested Nitrous Oxide as pain control
50
Horace Wells 1815-1848; Dentist
Noticed that a man under the influence of N2O had no recall of pain/injury
51
What was the result of Horace Wells demonstrating the use of N2O for an amputation @ Mass General?
The patient rolled around and groaned as if in pain, Wells was then ridiculed and this was shown as a failure
52
Who realized that the administration of nitrous + oxygen resulted in no cyanosis of the patient?
Dr. Andrews
53
Who invented the first anesthesia machine that had nitrous and oxygen chained together?
Hewitt
54
What was the major side effect of Ether use?
Massive nausea and vomiting
55
Crawford Long 1842
Delivered either for a patient with 2 vascular neck tumors
56
William Morton 1819-1868; Dentist
1846, 1st successful public demonstration of ether…vascular tumor of neck in sitting position
57
Dr. Robinson Squibb
Developed process for pure ether
58
Where was chloroform discovered?
Independently in 1831 by the USA, France, Germany, and Great Britain
59
Sir James Simpson 1847; Obstetrician in Scotland
Defined pain: “actual or potential tissue damage,” encountered religious opposition
60
Dr. John Snow - Anesthetist
"discovered” epidemiology when he traced London cholera outbreak to water source
61
First well-known person to have anesthesia for child birth administered by Dr. John Snow?
Queen Victoria
62
Guthrie, 1894
delayed chloroform hepatotoxicity in children
63
Levy (1856-1954
Light chloroform anesthesia and adrenaline….fatal vf in animals
64
What were deaths under chloroform use attributed to?
Overuse of the medication and lack of adequate supervsion
65
Characteristics attributed to Sister Mary Bernard in 1877
Low pay, Intelligent, Focus
66
Alice Magaw 1860-1928
“mother of anesthesia,” 14,000 open drop ether cases without death
67
Characteristics of Agatha Hodgins 1877-1945
Opened one of 1st nurse anesthesia schools, Taught in France, Developed nitrous/oxygen techniques, Founded AANA
68
Why is cyclopropane not on the market?
Violently explosive
69
Halothane
Halothane hepatitis, Slow onset, slow offset
70
Who realized that volatile anesthetics go to the brain and tissues?
Edmund Egar
71
Isoflurane (Suprane) characteristics
Oldest but not cheapest, slowest onset and slowest offset, less nausea and vomiting, quicker onset than halothane
72
Desflurane
rapid onset and offset, large quantity needed for anesthesia, does not sit in the fat, irritable to airway so not good for asthma or COPD
73
Sevoflurane
intermediate action between iso and des, used for kids, not irritable to airway, unstable in soda lime
74
What is Dr. Lister (Morton) famous for?
3 deaths during 1 amputation operation
75
George Crile (1864-1943)
Preemptive analgesia, local infiltration of procaine
76
Harvey Cushing (1869-1939)
Regional blocks prior to emergence from ether, Anesthetic records, BP/HR measurements
77
Adverse effects of neuroleptic anesthesia through medications such as raglan or anapsine
Blocked autonomic and endocrine response to stress, High incidence of awareness, dysphoria, extrapyramidal movements
78
What was cocaine utilized for?
Ophthalmic and sinus surgery
79
Dr. August Bier
1st spinal with cocaine, developed bier block
80
Bier block
Tourniquet utilized, lidocaine, numbs extremity
81
Preoperative period of anesthesia drugs
BZD, H1 and H2 blockers, bronchodilators
82
Maintenance phase of anesthesia
Inhalation drugs, neuromuscular blockers, pressors, blockers
83
Emergence phase of anesthesia
NMB reversal, local anesthetics
84
4 Phases of Anesthesia
Perop, maintenance, emergence and postop
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Stage 1 of Anesthesia
beginning of induction of general anesthesia to loss of consciousness 1st plane: no amnesia or analgesia 2nd plane: amnestic but only partially analgesic 3rd plane: complete analgesia and amnesia
86
Stage 2 of Anesthesia (MOST DANGEROUS STAGE)
loss of consciousness to onset of automatic breathing (irritable, dangerous stage), eyelash reflex disappears, coughing, vomiting, struggling may occur, irregular respirations with breath-holding Want to get through this stage quickly
87
Stage 3 of Anesthesia
onset of automatic respiration to respiratory paralysis (surgical plane)
88
Anesthesia Stage 3 Plane 1
automatic respiration to cessation of eyeball movements
89
Anesthesia Stage 3 Plane 2
cessation of eyeball movements to beginning of intercostal muscle paralysis
90
Anesthesia Stage 3 Plane 3
beginning to completion of intercostal muscle paralysis, pupils dilate Desired Plane prior to muscle relaxants
91
Anesthesia Stage 3 Plane 4
complete intercostal paralysis to diaphragmatic paralysis (apnea)
92
Stage 4 of Anesthesia
stoppage of respiration till death; Gone too far
93
What allows agonists/antagonists to be reversible?
The bond type of the molecule
94
What are the 3 types of bonds that substrates use to activate a receptor?
1. Ion 2. Hydrogen 3. Van der Waals
95
What does the drug effect relate to?
Number of bound receptors, the more the merrier
96
When will you see the greatest effect from a drug?
All of the receptors are bound
97
What type of receptor are we usually dealing with?
proteins
98
Can you overcome non-competitive antagonism?
No, you can only overcome competitive antagonism
99
What can cause the number of receptors to increase or decrease?
Comorbidities and drug therapies
100
What do we see happen to receptors when a patient chronically uses albuterol for asthma?
Downregulation of receptors due to repetition
101
What does drug concentration in the plasma tell us?
How fast a drug is being distributed and where it is going
102
Are anesthetics active in the plasma?
No
103
Where are the effector sites located for anesthetic drugs?
Brain, spinal cord, lungs
104
What type of pharmacology determines the concentration of a drug?
Pharmacokinetics
105
What is the 1 compartment model of distribution?
Concentration of drug is immediately diluted by the plasma by a central compartment in the first minute of admin that determines Vd
106
What is Vd?
Volume of distribution tells us if the drug prefers to stay in the plasma or distribute to other areas of the body
107
What is the sequence areas that blood flows starting from the venous blood in arm?
1. Venous blood in arm 2. Inferior vena cava 3. Right heart 4. Pulmonary vessels 5. Left heart 6. Aorita
108
What are 2 examples of vessel poor groups?
Ligaments and tendons
109
Why do men require more NMBD than women?
Larger amount of muscle mass in men
110
What makes propofol Vd 5000?
It is highly lipophilic
111
What increases the Vd?
Adding more areas where the drug is likely to go
112
What type of drugs primarily bind to albumin?
Acidic drugs
113
Where do alkaloid drugs primarily bind to?
A1-Acid Glycoprotein
114
What state of drug is able to cross cell membranes?
Free drugs
115
What state of drug, free or bound, determines concentration available to receptor (potency)
Free drug
116
Patient A shows to have more unbound drug than Patient B, which patient will show the greatest effect from the medication?
Patient A
117
4 Variables that would decrease amount of plasma proteins?
1. Age 2. Hepatic Disease 3. Renal failure 4. Pregnancy
118
What is the final free fraction of a drug who's normal free fraction is 2% when there is a net loss of 50% of proteins?
4%, which means the effect is increased
119
What type of Vd would drugs that have poor protein binding and lipid solubility show?
High volume of distribution, an example would be propofol
120
What type of Vd would drugs who are highly protein bound show?
Small volume distribution, an example would be warfarin
121
What does metabolism of a drug do?
Converts active, lipid soluble drugs to water soluble drugs to allow excretion of the drug through the kidneys
122
4 examples of drug metabolism?
1. Hepatic microsomal enzymes 2. Hoffman Elimination 3. Ester Hydrolysis 4. Tissue Esterase
123
3 Types of phase 1 reactions
1. Oxidation 2. Reduction 3. Hydrolysis
124
What does Phase I metabolism do to prepare for Phase II metabolism?
Makes the drug more polar
125
What occurs in Phase II metabolism?
Covalent link with a highly polar molecule to become water soluble through conjugation
126
4 Characteristics of CYP450 enzymes?
1. Large family 2. Membrane bound 3. Contains heme cofactor 4. Involves oxidation and reduction (Phase I)
127
What is the most common CYP450 enzymes?
CYP3A4, which metabolizes \>50% of drugs such as opioids, benzos, locals, immunosuppressants and antihistamines
128
When CYP450 is induced, what would you expect?
To have to increase the amount of administered to achieve the same effect as normal
129
What is an example of a drug that induces CYP450 enzymes?
Phenobarbital
130
What would you expect if CYP450 is inhibited?
The effect of drugs may last longer than desired
131
What is an example of a drug that inhibits CYP450?
Alcohol and grapefruit juice
132
What do you need for oxidation to occur?
An electron donor and oxygen
133
What is reduction in phase I metabolism?
Transfer of electrons directly to the substrate instead of to oxygen
134
What is phase I metabolism, reduction, good for?
Low PaO2
135
Where are drugs that undergo glucuronidation excreted?
Bile and urine
136
What is an example of a condition that interferes with conjugation?
Neonatal hyperbilirubinemia
137
What type of metabolism does not involve CYP enzymes?
Hydrolysis
138
Where does hydrolysis often occur and what type of bond does it usually occur at?
Often occurs outside of the liver and at ester bonds
139
3 examples of drugs that undergo hydrolysis
1. Succinylcholine (Anectin) 2. Esmolol (Brevibloc) 3. Ester Local Anesthetic (Procaine, Cocaine)
140
What are the Phase II enzymes?
"Transferases"
141
For \>50% of anesthetics, what is clearance rate proportional to?
Clearance rate is proportional to concentration; More drug/more clearance
142
Equation for rate of drug metabolism?
R = [Arterial blood flow = Q](C inflow - C outflow)
143
What does flow limited metabolism mean?
Arterial blood flow, Q, limits metabolic rate
144
What does capacity limited metabolism mean?
Livers ability to metabolize is the limiting factor, SE can build up overtime if re-administration of a drug is too soon
145
Which drugs, lipid/water soluble, are less likely to be reabsorbed by the kidneys?
Water soluble drugs
146
What effect does context sensitive half-time ignore?
Plasma-effect site disequilibrium
147
What increases the context sensitive half-time?
Longer infusion durations
148
What is an example of a drug class that are weak acids.
Barbiturates such as thiopental
149
What are examples of drug classes that would be considered weak bases?
Opioids and local anesthetics
150
What form of a drug is lipid soluble, non-ionized or ionized?
non-ionized
151
What form of a drug is active, non-ionized or ionized?
non-ionized
152
How are non-ionized drugs metabolized?
Hepatic metabolism
153
What is the mnemonic to figure out ionization vs non ionization?
Weak Acids, PK After pH Weak Bases, PK Before pH Nicely negative numbers are non-ionized
154
What chronic disease would display atypical enzymes?
Renal failure
155
3 reasons for varying drug responses in the elderly
1. Decreased cardiac output 2. Decreased protein binding 3. Increased body fat
156
Which enantiomer of ketamine is more potent with less delirium?
S-enantiomer
157
Which enantiomer of bupivicaine has 30% less cardiac toxicity?
L-Bupivicaine
158
Which isomer of atracurium lacks histamine effects?
Cisatracurium (Nimbex)
159
What benefit is there to using Xopenex over albuterol?
Xopenex shows no heart rate jump
160
Midazolam (doses)
Induction: 0.2-0.3 mg/kg IV over 30-60 seconds Sedation: 1-5mg IV (adults) Oral (Pedi): 0.25 - 0.5 mg/kg Post-Op Sedation: 1 - 7 mg/hr IV (max 2 - 3 days)
161
Diazepam (doses)
Anticonvulsant: 0.1 mg/kg IV Induction: 0.3 - 0.5 mg/kg IV (decrease for elderly/Liver Disease)
162
Lorazepam (doses)
1 - 4 mg IV (single dose)
163
Romazicon (doses)
0.2 mg IV then 0.1 mg q1min. until desired effect (1 mg max)
164
What are Freud's three levels of mind?
1. Conscious mind 2. Preconscious mind 3. Unconscious mind
165
What anesthetic drugs were used that showed changes in electrical activity on the EEG?
Chloroform and volatile anesthetics
166
What can the EEG be used for in terms of anesthesia?
Measure effects
167
What 2 factors related to EEG activity does anesthesia alter?
Cerebral blood flow and cerebral metabolic requirement of oxygen
168
What did processing the EEG give us?
Bispectral Analysis
169
What did BIS studies show when utilizing hypnotics?
BIS change correlated to patient movement
170
What did BIS studies show when utilizing high dose narcotics?
Less correlation between BIS and movement
171
At what level of BIS showed that a patient was not conscious?
BIS score of \<58
172
What did a BIS score of \<65 show?
Less than 5% chance of return to consciousness within 50 seconds
173
What should the EMG show on a BIS during a procedure?
0, if it is above 0 then it indicates lots of patient movement
174
What range of BIS correlates with relatively no recall of the procedure?
40-60
175
What would Ketamine give us on a BIS monitor? Beta-blockers?
Ketamine - false high Beta blockers - false low
176
When is the best time to give benzodiazepines?
Pre-op environment, especially with patients who have chronic anxiety
177
What do benzos cause from the spinal cord?
Skeletal muscle relaxation
178
What is the only thing that causes retrograde amnesia?
Electroconvulsive therapy
179
What does it mean when we say benzodiazepines cause anterograde amnesia?
Patients will not remember anything after the medication has been administered, the amnesic effect will last longer than sedation
180
When metabolizing benzos, what do they lack compare to barbiturates?
They do not have hepatic microsomal enzymes
181
Which benzodiazepine has the shortest elimination half time?
Midazolam
182
Which benzodiazepines have greater context sensitive half times than midazlolam?
Diazepam and Lorazepam, this effect makes them more attractive for sedation postop
183
What is the mechanism of action for benzos?
They facilitate GABA agonism, allowing for enhanced opening of Cl- channels
184
What effect does the GABA alpha-1 site have?
sedative, amnesic, anticonvulsant
185
Where are the GABA alpha-1 sites found to have effect?
cerebral cortex, cerebellar cortex, thalamus
186
What effect does the GABA alpha-2 site have?
Anxiolytic, anti-hyperalgesia, skeletal muscle relaxation
187
Where are the GABA alpha-2 sites found to have effect?
Hippocampus, amygdala
188
What are 4 other substrates that bind to GABA receptor binding sites and also have a synergistic effect?
1. Barbiturates 2. Etomidate 3. Propofol 4. Alcohol
189
What do benzos bind to in the plasma?
Albumin
190
Effects of chronic renal failure/cirrhosis on benzodiazepine metabolism?
More free drug, making it more potent
191
What do we tell the patient if we do not administer benzos in the pre-op area?
The patient will remember the trip to the OR and going to sleep
192
What effect do benzos have on EEG's?
decrease alpha and fast-beta activity, meaning the EEG is slower
193
Do benzos show tachyphylaxis?
Benzos do not show tolerance per EEG
194
What does it mean that benzos do not produce isoelectric states on the EEG?
They have a high margin of safety
195
What pathway is Lorazepam (Ativan) metabolized by?
Glucuronidation, it does not have any active metabolites and is safer to give the elderly
196
What are the effects of metabolism on Diazepam/Midazolam?
Active metabolites
197
What is the risk factor for postoperative confusion when giving benzos?
Daily use \> 1 year
198
What effect if any do benzos have on platelets?
Benzos have been shown in the lab to inhibit platelet aggregating factor
199
3 Important facts about midazolam (versed)
1. Imidazole ring 2. 2-3x as potent as diazepam d/t greater affinity for receptor 3. Amensia \> sedation
200
What are the two variations of pH dependent ring opening of midazolam?
pH \< 3.5, ring opens and is water soluble pH \>4.0 ring closes and is lipid soluble
201
What is the onset of action and peak effect time of midazolam?
onset of action: 1-2 minutes IV peak effect time: 5 minutes
202
What is the issue with giving midazolam oral?
Significant 1st pass effect
203
What is the elimination half time of midazolam?
2 hours, this effect is doubled in elderly patients
204
What enzymes metabolize midazolam?
CYP3A4
205
What is the active metabolite of midazolam and where is it eliminated through?
1-hydroxymidazolam is cleared through the kidneys
206
5 drugs that inhibit CYP40 enzymes
1. Cimetidine 2. Erthromycin 3. CCB 4. Antifungals 5. Fentanyl
207
What effect does not allow midazolam to produce an isoelectric EEG?
Ceiling effect
208
What is the effect of midazolam on ICP?
No change in ICP, making it good for induction with neuro pathologies
209
What is the effect of midazolam on the pulmonary system?
Dose dependent decreases in ventilation, which is exaggerated with opioids/CNS depressant drugs. Midazolam also depresses swallowing reflective and decrease upper airway activity.
210
What is the effect of midazolam on the CV system?
Dose dependent increases in HR and decreases in BP. No change in cardiac output, hypotension is enhanced with hypovolemic patients. No BP/HR response to intubation
211
When and what route do we give midazolam to pedi patients?
Oral admin 30 minutes before induction
212
What effect does midazolam have on volatile anesthetics?
Dose dependent decreases in volatile requirements
213
What does clearance of midazolam depend on?
Hepatic metabolism, the activite metabolites will accumulate and delay awakening
214
What is the recommended time period for post-op sedation with midazolam per the Society of Critical Care Medicine?
2-3 days
215
How is the duration of action of diazepam when compared to midazolam?
much longer
216
When diazepam is mixed in propylene glycol, what is the side effect?
pain on injection/glycol toxicity
217
When diazepam is mixed with soybean formula, what is the side effect?
less painful
218
What is the onset of action and elimination half time of diazepam?
onset of action: 1-5 minutes elimination half time: 20-40 hours
219
What does diazepam bind to in the plasma?
Extensively protein bound
220
How is the duration of action and elimination half time of diazepam when compared to lorazepam?
Duration of action is shorter and elimination half time is longer. Diazepam dissociates from GABA faster than lorazepam
221
What pathway does diazepam follow for metabolism?
CYP3A
222
What is the active metabolite of diazepam?
Desmethyldiazepam and oxazepam
223
When do we se a return of drowsiness with diazepam?
6-8 hours
224
Where are the active metabolites of diazepam excreted?
in the urine
225
What can diazepam abolish at 0.1mg/kg IV?
DT's, Status epileptics, lidocaine toxicity
226
What benzodiazepine can produce an isoelectric EEG?
Diazepam
227
What are the effect of diazepam on ventilation?
Minimal effects: 1. Slight decrease Vt 2. After 0.2 mg/kg IV increases in PaCO2 3. Exaggerated with opioids, alcohol, COPD
228
What can reverse the ventilatory depressant effects of diazepam?
Surgical stimulation
229
Cardiovascular effects of diazepam?
Minimal decreases in BP, CO and SVR with induction doses. BP changes are additive with opioids
230
What benzodiazepine has transient depression of baroreceptor mediated HR response?
diazepam
231
What are the neuromuscular effects of diazepam?
Skeletal muscle tone decreased through spinal neurons
232
How much do we decrease the dose of diazepam by in the elderly, liver disease patients or in the presence of opioids?
25-50% dose reduction
233
What does lorazepam resemble?
Oxazepam, it has an extra Cl- atom
234
When compared to midazolam and diazepam, how are the sedative and amnestic effects of lorazepam?
more potent
235
What is lorazepam prepared in?
Propylene glycol
236
Why does lorazepam have slower entrance to the CNS than midazolam or diazepam?
lower lipid solubility
237
What is the peak effect and elimination half time of lorazepam?
Peak effect: 20-30 minutes (1-4mg IV) Elimination half time is 14 hours (slower than midazolam)
238
Which benzodiazepine is less affected by hepatic function, age, drugs (cimetidine)?
lorazepam
239
What does flumazenil antagonize with the BZD/opioid combo?
ventilatory depression
240
What does flumazenil prevent/reverse?
All agonist activity of Benzos
241
What is flumazenil a derivative of?
1,4 imidazobenzodiazepine
242
What is flumazenil metabolized by?
Hepatic microsomal enzymes into inactive metabolites
243
When is flumazenil contraindicated?
Use of antiepileptic drugs and predicates acute withdrawal seizures
244
When reversing benzos with flumazenil, will we see acute anxiety, hypertension, tachycardia, or change in MAC?
No
245
What did Hippocrates contribute to anesthesia?
1. Accommodate the operator 2. Avoid sinking down and turning away
246
What did Dr. Koller contribute to anesthesia?
Utilized cocaine as an anesthetic for eye surgery (Collegague of Sigmund Freud)
247
What did Dr. Halsted contribute to anesthesia?
1st regional mandibular nerve block with cocaine
248
What does Histamine induce?
endogenous substance involving basophils and mast cells Contraction of SM in airways Acid secretion in the stomach Neurotransmitter release in CNS.
249
H1 Receptors (what do they do when activated)
associated with hyperalgesia and inflammatory pain. weak anticholinergic (anti-muscarinic) activity
250
3 things that histamine induces in the body?
1. Contraction of smooth muscles in airway 2. Secretion of acid in the stomach 3. Release of neurotransmitters in CNS
251
2 Process that H1 receptors are involved in
1. Hyperalgesia and inflammatory pain 2. Weak anticholinergic (Anti-muscarinic) activity
252
H1 Receptor Antagonists (Drugs and side effects)
Diphenhydramine Promethazine (they are effective AND inexpensive) Side effects include: Blurred vision, urinary retention, dry mouth, drowsiness (1st gen), heart block.
253
What is the greatest side effect from H1 receptor antagonists and why do we see this effect?
Sleepiness because they cross the blood brain barrier
254
What are the three MOA's thought to occur when we give an H1 receptor antagonist?
1. Receptors in vestibular system; effective for motion sickness 2. Allergic Rhinoconjunctivitis 3. Helps w/ anaphylactic reactions
255
H2 Receptors (when activated they...)
elevate Cyclic-AMP increase acid production
256
H2 Receptor Antagonists (MOA)
decrease gastric volume, but do NOT effect pH
257
Estimated half time and onset of action of Promethazine (Phenergan)?
half time: 9-16 hours onset of action: 5 minutes
258
Dose of Promethazine (Phenergan)
12.5-25mg
259
What precaution was place on phenergan as a black box warning in 2009?
Gangrene if promethazine infiltrated
260
Dose of Promethazine (Phenergan)
12.5-25mg
261
Histamine releasing drugs
Morphine Mivacurium Protamine Atracurium we need to antagonize both receptors (H1 and H2) to reduce CV effects. (H2 treatment alone increases CV side effects)
262
Proton Pump Inhibitors (PPIs MOA)
irreversibly binds to acid secreting "pumps" stopping the movement of protons across the gastric parietal cells decrease gastric volume AND lower pH
263
PPIs (Drugs and side effects)
Omeprazole Pantoprazole Lansoprazole Dexlansoprazole Side effects inlucde: bone fx, Lupus, acute interstitial nephritis, C-Diff, B-12/Mg deficiency, inhibits warfarin metabolism
264
Omeprazole (PPI)
released as prodrug in the small intestine (EC), returns to parietal cells. CYP450 metabolized. significantly controls daytime, nocturnal, and meal time acid secretion. Dose: 40 mg in 100 ml over 30 minutes. (PO give \>3hrs earlier) but needs up to 5 days to take full effect.
265
Omeprazole (side effects)
Side effects include: HA, Agitation, confusion, ABD pain, N/V, Flatulence
266
Dose of diphenhydramine?
25-50 mg
267
What reflex might be inhibited with diphenhydramine use?
Afferent arc of oculo-emetic reflex
268
Does benadryl exacerbate opioid-induced depression of hypoxic response?
no
269
Effects of H2 receptor antagonists?
1. Decreased gastric volume 2. No effect on gastric pH
270
4 Side effects of H2 receptor antagonists
1. Diarrhea 2. Headache 3. Skeletal muscle pain if given too quickly 4. Weakend gastric mucosa to bacteria in prolonged administration
271
3 Examples of H2 receptors antagonists
1. Cimetidine (Tagamet) 2. Ranitidine (Zantac) 3. Famotidine (Pepcid)
272
How is cimetidine metabolized and excreted?
In the liver by CYP450 and cleared in the urine
273
What effect does cimetidine have on CYP450?
Reduces metabolism
274
7 drugs associated with CYP450 metabolism that we don't want to give concurrently with Tagamet?
1. Warfarin 2. Phenytoin 3. Lidocaine 4. Tricyclics 5. Propranolol 6. Nifedipine 7. Meperidine
275
Adverse effects associated with cimetidine?
1. HA 2. Confusion (Crosses BBB) 3. Bradycardia 4. Hypotension
276
Normal dose of Cimetidine and renal impairment dose?
Dose: 150-300 mg IV Renal impairment: 1/2 dose
277
Metabolism and excretion meshing for ranitidine and famotidine?
Hepatic metabolism and renal clearance
278
4 known drugs that cause histamine release?
1. Protamine 2. Atracurium 3. Mivacurium 4. Morphine
279
Normal dose and renal impairment dose for ranitidine?
Normal: 50mg diluted to 20CC over 2 min Renal impairment: 1/2 dose
280
Which H2 receptor antagonist has no effect on CYP enzymes?
Famotidine (Pepcid)
281
Normal dose and renal impairment dose for famotidine (Pepcid)?
Normal: 20mg IV Renal impairment: 1/2 dose
282
What are proton pump inhibitors most effective for treating?
1. Controlling gastric acidity 2. Decreasing gastric volume
283
Which Histamine receptor antagonist, if given alone in anaphylaxis, has been shown to worse symptoms?
H2
284
6 pathologies that PPI's have been associated with?
1. Bone fractures 2. SLE 3. Acute intestinal nephritis 4.. C-diff 5. Vitamin B12/Magnesium Deficiency 6. Inhibits warfarin metabolism
285
What are proton pump inhibitors most effective for treating?
1. Controlling gastric acidity 2. Decreasing gastric volume
286
3 actions of omeprazole
1. Released in small intestine (prodrug) 2. Returns to parietal cells 3. Acid-inhibition increases with repeated dosing
287
6 pathologies that PPI's have been associated with?
1. Bone fractures 2. SLE 3. Acute intestinal nephritis 4.. C-diff 5. Vitamin B12/Magnesium Deficiency 6. Inhibits warfarin metabolism
288
4 examples of PPIs
1. Omeprazole (Prilosec) 2. Pantoprazole (Protonix) 3. Lansoprazole (Prevacid) 4. Dexlansoprazole (Dexilent)
289
When do we significantly greater control with prilosec administration?
Daytime, nocturnal and meal acid secretion more so than h2 drugs
290
What is omeprazole (Prilosec) metabolized by?
CYP enzymes, but causes no clinically significant inhibition of other drugs
291
Dose of omeprazole?
40 mg in 100 cc NS over 30 minutes or PO \>3 hours prior
292
SE associated with omeprazole?
1. HA 2. Agitation 3. Confusion 4. ABDOMINAL PAIN 5. N/V 6. Flatulence
293
What is pantoprazole (protonix) metabolized by?
CYP enzymes in the liver
294
What H2 receptor antagonist does protonix work just as fast as?
Ranitidine (Zantac)
295
How long prior to surgery should we give pantoprazole to see a decrease in gastric volume and pH
1 hour prior
296
Dose of pantoprazoe (protonix)
40 mg in 100 mL over 2-15 minutes
297
Treatment of choice for GERD?
PPI (increased pH and decreased gastric volume)
298
Treatment of choice for gastroduodenal ulcers?
PPI
299
Treatment of choice for aspiration pneumonitis?
H2 blockers b/c they work faster
300
Treatment of choice for acute upper GI bleed?
PPI infusion post EGD tx
301
Treatment of choice for aspiration pneumonitis?
H2 blockers b/c they work faster
302
Promethazine (H1 receptor antagonist)
Elimination 1/2 time: 9 - 16 hours Dose: 12.5 - 25 mg IV (onset 5 minutes) effective for acute N/V, may reduce pain levels watch for IV infiltration street tip: Key ingredient in Lean.
303
What is an example of an antacid?
Sodium citrate (Bicitra)
304
What are the two side effects seen from long term antacid us?
1. Acid breakdown of food inhibited 2. Acid rebound can occur
305
3 side effects associated with magnesium based antacids?
1. Osmotic diarrhea 2. Neurologic impairment 3. Neuromuscular impairment (diminished deep tendon reflexes)
306
3 side effects associated with calcium based antacids?
1. Hypercalcemia 2. Kidney stones 3. Dysrythmias
307
Non-particulate antacids neutralize acid, what cases are these good for?
1. Trauma 2. Obese patients with reflux 3. Emergent c-sections
308
2 effects seen when using Sodium Citrate (Bicitra)
1. Protection against aspiration pneumonia 2. Increases intra-gastric volume up to 30cc
309
What are the two effects seen from long term antacid us?
1. Acid breakdown of food inhibited 2. Acid rebound can occur
310
3 effects associated with magnesium based antacids?
1. Osmotic diarrhea 2. Neurologic impairment 3. Neuromuscular impairment (diminished deep tendon reflexes)
311
3 Patient populations that we assume have a full stomach?
1. Insulin dependent diabetics d/t delayed gastric motiity 2. Trauma patients 3. Pregnant women \>12 weeks gestation
312
Effect associated with Sodium based antacids?
Increased sodium load
313
Dose and Onset of action of sodium citrate?
dose: 15-30 mL PO onset of action: Immediately
314
When do you lose effectiveness of sodium citrate?
30-60 minutes after administration
315
What major reaction do we see with administration of metoclopromide (raglan) and how do we dampen this?
Extrapyramidal reactions d/t crossing the BBB and we can dampen by given benadryl first
316
What is the only drug cleared by the FDA for diabetics gastroparesis?
Reglan
317
3 examples of dopamine blockers?
1. Metocolopramide (Reglan) 2. Domperidone [Associated with cardiac arrest) 3. Droperidol (Inapsine)
318
SE associated with reglan?
1. Abdominal cramping (if rapid IV admin) 2. Hypotension and HR changes 3. Extra pyramidal symptoms and increased sedation with CNS deppressants
319
Dose of metoclopramide and when to administer it?
10-20mg IV over 3-5 minutes, 15-30 minutes prior to induction
320
Why is domperidone not FDA approved?
It is associated with Dysrhythmias and sudden death
321
What does domperidone increase the secretion of?
Prolactin secretion by pituitary gland
322
Why is domperidone not FDA approved?
It is associated with Dysrhythmias and sudden death
323
H2 Receptor Antagonists (MOA)
decrease gastric volume, but do NOT effect pH
324
What two diagnosis was droperidol (inapsine) developed to treat?
1. Schizophrenia 2. Psychosis
325
What is the blackbox warning associated with droperidol?
QT prolongation with higher doses such as 2.5-5mg IV
326
Dose of droperidol (Inapsine)
0.625-1.25mg IV
327
Where is serotonin released from in the small intestine?
Chromaffin cells
328
Where are the 5HT3 receptors found?
Kidneys, colon, liver, lung, stomach
329
Where are high concentration of 5HT3 receptors found that are linked to vomiting?
Brain and GI tract
330
5HT3 antagonists have almost no side effects, were great for PONV and were originally use in the treatment of what?
Chemotherapy and Radiation therapy related N/V (CIV)
331
What are 5HT3 receptor antagonist NOT effective in treating?
motion sickness/vestibular stimulation
332
3 Examples of 5HT3 receptor antagonist?
1. Ondansetron (Zofran) [Works the best] 2. Granisetron (Kytril) 3. Dolasteron (Anzemet)
333
Which 5HT3 antagonist was the first of its kind and does not have an CNS effects?
Ondansetron (Zofran)
334
Dose and plasma half life of ondansetron (zofran)?
Dose: 4-8mg IV Plasma 1/2: 4 hours
335
What are three possible MOA's of corticosteroids?
1. Glucocorticoid receptor in nucleus tractus solitarius 2. Increase effectiveness for 5HT3 antagonists and droperidol 3. Possible inhibition of prostaglandin synthesis and endorphin release
336
What receptor is droperidol (inapsine) a strong antagonists of?
D2 receptors
337
What annoying side effect is associated with dexamethasone admin?
perineal burning/itching
338
What is the dose if corticosteroids are used for PONV?
4-8 mg IV
339
What is the delay in onset of dexamethasone (decahedron) and how long does its efficacy persist?
Delay in onset of 2 hours and efficacy persists for 24 hours
340
What annoying side effect is associated with dexamethasone admin?
perineal burning/itching
341
What class of drug is scopolamine?
Competitive muscarinic antagonist
342
Where is the thinnest area available for a scopolamine patch?
Post auricular area (behind the ear)
343
Priming dose of scopolamine?
1.5mg @ 5mcg/hour
344
SE associated with scopolamine patches?
Dilated pupils and light sensitivity
345
How long does 1 scopolamine patch last?
24-72 hours
346
Priming dose of scopolamine?
1.5mg @ 5mcg/hour
347
What 3 effects are seen cellularly when giving bronchodilators?
1. Activate cAMP 2. Decrease Calcium ion entry 3. Decrease contractile protein sensitivity to Calcium ions
348
Which version of bronchodilators is more lipophilic? SABA or LABA?
LABA (long acting bronchodilator)
349
What is the advantage of using levo-albuterol (xopenex) over albuterol (proventil)?
Xopenex does not see as big of a jump in HR
350
H2 Receptor Antagonists (Drugs and Side Effects)
Cimetidine Ranitidine Famotidine Side effects include: Diarrhea, HA, Skeletal muscle pain, Weakened gastric mucosa to bacteria (prolonged use)
351
Cimetidine (H2 receptor antagonist)
metabolized by CYP450, cleared in urine Dose: 150 - 300 mg IV (half for renal disease) binds heavily to heme group of CYP450 (inhibits) Side effects include: HA, confusion (crosses BBB), bradycardia, hypotension
352
Ranitidine (H2 receptor antagonist)
hepatic metabolized, urine cleared (moderate CYP450 binding) Dose: 50 mg diluted to 20 ml over 2 minutes (half for renal disease)
353
Famotidine (H2 receptor antagonist)
hepatic metabolism, urine cleared (none/least CYP450 binding) Dose: 20 mg IV (half for renal disease)
354
Histamine releasing drugs
Morphine Mivacurium Protamine Atracurium we need to antagonize both receptors (H1 and H2) to reduce CV effects. (H2 treatment alone increases CV side effects)
355
Proton Pump Inhibitors (PPIs MOA)
irreversibly binds to acid secreting "pumps" stopping the movement of protons across the gastric parietal cells decrease gastric volume AND increases pH
356
PPIs (Drugs and side effects)
Omeprazole Pantoprazole Lansoprazole Dexlansoprazole Side effects inlucde: bone fx, Lupus, acute interstitial nephritis, C-Diff, B-12/Mg deficiency, inhibits warfarin metabolism
357
Omeprazole (PPI)
released as prodrug in the small intestine (EC), returns to parietal cells. CYP450 metabolized. significantly controls daytime, nocturnal, and meal time acid secretion. Dose: 40 mg in 100 ml over 30 minutes. (PO give \>3hrs earlier) but needs up to 5 days to take full effect.
358
Omeprazole (side effects)
Side effects include: HA, Agitation, confusion, ABD pain, N/V, Flatulence
359
Pantoprazole (PPI)
CYP metabolism in liver. works fairly quickly (1 hour prior) to decrease gastric volume. no drug interactions Dose: 40 mg in 100 ml over 2 - 15 minutes.
360
Induction of anesthesia drugs
Etomidate, ketamine, propofol, narcotics
