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Advanced Pharmacology 2 > Exam 1 Kane > Flashcards

Exam 1 Kane Flashcards

1
Q

A drug induced loss of consciousness during which pts are not arousable, even by painful stimulation.

A

General Anesthesia

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2
Q

A medication that includes more than one enantiomer

A

racemic

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3
Q

Agents with chiral molecules that are mirror images of each other are known as

A

enantiomers

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4
Q

An agent that activates a specific molecule in a biologic system

A

Agonist

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5
Q

Half-life is known as the amt of time to clear ½ of drug from the

A

body

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6
Q

Describe Minimal Sedation

A

anxiolysis; normal response to verbal commands, airway unaffected, ventilation unaffected, cardiac unaffected

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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

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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,

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9
Q

Describe allodynia

A

Due to a Stimulus that does not normally cause pain

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10
Q

The term that describes Increased pain perception from a stimulus that normally provokes pain

A

Hyperalgesia

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11
Q

Increased transduction/transmission of nociception; the process that causes hyperalgesia or allodynia

A

sensitization

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12
Q

Pain caused by a lesion or disease of somatosensory nervous system ; Characterized by reduced sensory and nociceptive thresholds

A

Neuropathic Pain

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13
Q

Pain transmitted to brain through spinal or cranial nerves

A

Somatic Pain

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14
Q

Pain transmitted to brain through autonomic nerves (internal organs)

A

visceral pain

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15
Q

Pain in the distribution of a nerve or group of nerves

A

neuralgia pain

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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

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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

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18
Q

Two agents administered at the same time who potentiate each other 1+1=3

A

Synergistic

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19
Q

Agents that activates a specific molecule but does not act at the SAME binding site as the neurotransmitter in question

A

Allosteric

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20
Q

Acquired hyporeactivity to an agent

A

Tolerance

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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

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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

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23
Q

Acquire hyporeactivity to an agent that occurs very rapidly

A

Tachyphylaxis

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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

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25
Q

An agent that activates or inhibits an action but does not have a high affinity or efficacy for the desired effect

A

Partial

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26
Q

That action of specific molecules are inhibited or blocked by

A

Antagonist

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27
Q

The amount of drug totally cleared from the plasma over time and expressed in L/min

A

Clearance

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28
Q

The dose required to produce a therapeutic response is called

A

Potency

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29
Q

The inability to recall past experiences

A

Amnesia

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30
Q

The maximum therapeutic effect of a drug is known as

A

Efficacy

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31
Q

Which type of pain is described as “unpleaseant sensory and emotional experiences with actual or potential tissue damage” ?

A

both acute and chronic pain

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32
Q

Which type of pain is said to exist BEYOND the healing process

A

Chronic pain

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33
Q

Therapeutic index

A

Ratio between LD50/ED50 denoting the relative safety of the medication. The higher the ratio the safer the drug

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34
Q

Recall

A

Conscious memory

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35
Q

Chirality

A

subset of stereochemistry that has a center or centers of 3 dimensional asymmetry

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36
Q

Stereochemistry

A

the study of how molecules are structured in three dimensions

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37
Q

Pharmacodynamics

A

Study of the intrinsic sensitivity or responsiveness of the body to a drug and mechanisms by which theses effects occur.

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38
Q

Context-sensitive half-time

A
  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.
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39
Q

First-order processes

A

Processes where the rate of change varies over time. Processes that occur at a rate proportional to the amount.

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40
Q

Zero-order processes

A

Processes where the rate of change is constant

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41
Q

Vessel rich group

A

Tissues that receive the bulk of arterial blood flow

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42
Q

Pharmacokinetics

A

The quantitative study of the absorption, distribution, metabolism and excretion of injected and inhaled drugs and their metabolites

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43
Q

Inverse agonists

A

Bind at the same site of the agonist but produce the opposite effect of the agonist. Turn off constitutive activity of the receptor

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44
Q

Regional Anesthesia

A

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

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45
Q

Dioscorides 40-90 AD (surgeon in NERO’s army)

A

Materia Medica; Mandragora and wine (harry potter thing) – hallucinogenic, human shaped, magical

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46
Q

What is Ether the Greek word for?

A

Ignite

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47
Q

Sir Christopher Wren and Robert Boyle (1650s)

A

Utilized a goose quill as an IV to give a dog alcohol, probably the first sense of pharmacokinetics

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48
Q

Joseph Priestly 1773

A

Discovers oxygen and nitrous oxide

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49
Q

Humphry Davy 1800

A

Discovered potassium, sodium, calcium, magnesium and suggested Nitrous Oxide as pain control

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50
Q

Horace Wells 1815-1848; Dentist

A

Noticed that a man under the influence of N2O had no recall of pain/injury

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51
Q

What was the result of Horace Wells demonstrating the use of N2O for an amputation @ Mass General?

A

The patient rolled around and groaned as if in pain, Wells was then ridiculed and this was shown as a failure

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52
Q

Who realized that the administration of nitrous + oxygen resulted in no cyanosis of the patient?

A

Dr. Andrews

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53
Q

Who invented the first anesthesia machine that had nitrous and oxygen chained together?

A

Hewitt

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54
Q

What was the major side effect of Ether use?

A

Massive nausea and vomiting

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55
Q

Crawford Long 1842

A

Delivered either for a patient with 2 vascular neck tumors

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56
Q

William Morton 1819-1868; Dentist

A

1846, 1st successful public demonstration of ether…vascular tumor of neck in sitting position

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57
Q

Dr. Robinson Squibb

A

Developed process for pure ether

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58
Q

Where was chloroform discovered?

A

Independently in 1831 by the USA, France, Germany, and Great Britain

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59
Q

Sir James Simpson 1847; Obstetrician in Scotland

A

Defined pain: “actual or potential tissue damage,” encountered religious opposition

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60
Q

Dr. John Snow - Anesthetist

A

“discovered” epidemiology when he traced London cholera outbreak to water source

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61
Q

First well-known person to have anesthesia for child birth administered by Dr. John Snow?

A

Queen Victoria

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62
Q

Guthrie, 1894

A

delayed chloroform hepatotoxicity in children

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63
Q

Levy (1856-1954

A

Light chloroform anesthesia and adrenaline….fatal vf in animals

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64
Q

What were deaths under chloroform use attributed to?

A

Overuse of the medication and lack of adequate supervsion

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65
Q

Characteristics attributed to Sister Mary Bernard in 1877

A

Low pay, Intelligent, Focus

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66
Q

Alice Magaw 1860-1928

A

“mother of anesthesia,” 14,000 open drop ether cases without death

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67
Q

Characteristics of Agatha Hodgins 1877-1945

A

Opened one of 1st nurse anesthesia schools, Taught in France, Developed nitrous/oxygen techniques, Founded AANA

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68
Q

Why is cyclopropane not on the market?

A

Violently explosive

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69
Q

Halothane

A

Halothane hepatitis, Slow onset, slow offset

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70
Q

Who realized that volatile anesthetics go to the brain and tissues?

A

Edmund Egar

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71
Q

Isoflurane (Suprane) characteristics

A

Oldest but not cheapest, slowest onset and slowest offset, less nausea and vomiting, quicker onset than halothane

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72
Q

Desflurane

A

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

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73
Q

Sevoflurane

A

intermediate action between iso and des, used for kids, not irritable to airway, unstable in soda lime

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74
Q

What is Dr. Lister (Morton) famous for?

A

3 deaths during 1 amputation operation

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75
Q

George Crile (1864-1943)

A

Preemptive analgesia, local infiltration of procaine

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76
Q

Harvey Cushing (1869-1939)

A

Regional blocks prior to emergence from ether, Anesthetic records, BP/HR measurements

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77
Q

Adverse effects of neuroleptic anesthesia through medications such as raglan or anapsine

A

Blocked autonomic and endocrine response to stress, High incidence of awareness, dysphoria, extrapyramidal movements

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78
Q

What was cocaine utilized for?

A

Ophthalmic and sinus surgery

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79
Q

Dr. August Bier

A

1st spinal with cocaine, developed bier block

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80
Q

Bier block

A

Tourniquet utilized, lidocaine, numbs extremity

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81
Q

Preoperative period of anesthesia drugs

A

BZD, H1 and H2 blockers, bronchodilators

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82
Q

Maintenance phase of anesthesia

A

Inhalation drugs, neuromuscular blockers, pressors, blockers

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83
Q

Emergence phase of anesthesia

A

NMB reversal, local anesthetics

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84
Q

4 Phases of Anesthesia

A

Perop, maintenance, emergence and postop

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85
Q

Stage 1 of Anesthesia

A

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

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86
Q

Stage 2 of Anesthesia (MOST DANGEROUS STAGE)

A

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

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87
Q

Stage 3 of Anesthesia

A

onset of automatic respiration to respiratory paralysis (surgical plane)

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88
Q

Anesthesia Stage 3 Plane 1

A

automatic respiration to cessation of eyeball movements

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89
Q

Anesthesia Stage 3 Plane 2

A

cessation of eyeball movements to beginning of intercostal muscle paralysis

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90
Q

Anesthesia Stage 3 Plane 3

A

beginning to completion of intercostal muscle paralysis, pupils dilate Desired Plane prior to muscle relaxants

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91
Q

Anesthesia Stage 3 Plane 4

A

complete intercostal paralysis to diaphragmatic paralysis (apnea)

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92
Q

Stage 4 of Anesthesia

A

stoppage of respiration till death; Gone too far

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93
Q

What allows agonists/antagonists to be reversible?

A

The bond type of the molecule

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94
Q

What are the 3 types of bonds that substrates use to activate a receptor?

A
  1. Ion 2. Hydrogen 3. Van der Waals
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95
Q

What does the drug effect relate to?

A

Number of bound receptors, the more the merrier

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96
Q

When will you see the greatest effect from a drug?

A

All of the receptors are bound

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97
Q

What type of receptor are we usually dealing with?

A

proteins

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98
Q

Can you overcome non-competitive antagonism?

A

No, you can only overcome competitive antagonism

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99
Q

What can cause the number of receptors to increase or decrease?

A

Comorbidities and drug therapies

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100
Q

What do we see happen to receptors when a patient chronically uses albuterol for asthma?

A

Downregulation of receptors due to repetition

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101
Q

What does drug concentration in the plasma tell us?

A

How fast a drug is being distributed and where it is going

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102
Q

Are anesthetics active in the plasma?

A

No

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103
Q

Where are the effector sites located for anesthetic drugs?

A

Brain, spinal cord, lungs

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104
Q

What type of pharmacology determines the concentration of a drug?

A

Pharmacokinetics

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105
Q

What is the 1 compartment model of distribution?

A

Concentration of drug is immediately diluted by the plasma by a central compartment in the first minute of admin that determines Vd

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106
Q

What is Vd?

A

Volume of distribution tells us if the drug prefers to stay in the plasma or distribute to other areas of the body

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107
Q

What is the sequence areas that blood flows starting from the venous blood in arm?

A
  1. Venous blood in arm 2. Inferior vena cava 3. Right heart 4. Pulmonary vessels 5. Left heart 6. Aorita
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108
Q

What are 2 examples of vessel poor groups?

A

Ligaments and tendons

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109
Q

Why do men require more NMBD than women?

A

Larger amount of muscle mass in men

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110
Q

What makes propofol Vd 5000?

A

It is highly lipophilic

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111
Q

What increases the Vd?

A

Adding more areas where the drug is likely to go

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112
Q

What type of drugs primarily bind to albumin?

A

Acidic drugs

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113
Q

Where do alkaloid drugs primarily bind to?

A

A1-Acid Glycoprotein

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114
Q

What state of drug is able to cross cell membranes?

A

Free drugs

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115
Q

What state of drug, free or bound, determines concentration available to receptor (potency)

A

Free drug

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116
Q

Patient A shows to have more unbound drug than Patient B, which patient will show the greatest effect from the medication?

A

Patient A

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117
Q

4 Variables that would decrease amount of plasma proteins?

A
  1. Age 2. Hepatic Disease 3. Renal failure 4. Pregnancy
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118
Q

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?

A

4%, which means the effect is increased

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119
Q

What type of Vd would drugs that have poor protein binding and lipid solubility show?

A

High volume of distribution, an example would be propofol

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120
Q

What type of Vd would drugs who are highly protein bound show?

A

Small volume distribution, an example would be warfarin

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121
Q

What does metabolism of a drug do?

A

Converts active, lipid soluble drugs to water soluble drugs to allow excretion of the drug through the kidneys

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122
Q

4 examples of drug metabolism?

A
  1. Hepatic microsomal enzymes 2. Hoffman Elimination 3. Ester Hydrolysis 4. Tissue Esterase
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123
Q

3 Types of phase 1 reactions

A
  1. Oxidation 2. Reduction 3. Hydrolysis
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124
Q

What does Phase I metabolism do to prepare for Phase II metabolism?

A

Makes the drug more polar

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125
Q

What occurs in Phase II metabolism?

A

Covalent link with a highly polar molecule to become water soluble through conjugation

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126
Q

4 Characteristics of CYP450 enzymes?

A
  1. Large family 2. Membrane bound 3. Contains heme cofactor 4. Involves oxidation and reduction (Phase I)
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127
Q

What is the most common CYP450 enzymes?

A

CYP3A4, which metabolizes >50% of drugs such as opioids, benzos, locals, immunosuppressants and antihistamines

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128
Q

When CYP450 is induced, what would you expect?

A

To have to increase the amount of administered to achieve the same effect as normal

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129
Q

What is an example of a drug that induces CYP450 enzymes?

A

Phenobarbital

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130
Q

What would you expect if CYP450 is inhibited?

A

The effect of drugs may last longer than desired

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131
Q

What is an example of a drug that inhibits CYP450?

A

Alcohol and grapefruit juice

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132
Q

What do you need for oxidation to occur?

A

An electron donor and oxygen

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133
Q

What is reduction in phase I metabolism?

A

Transfer of electrons directly to the substrate instead of to oxygen

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134
Q

What is phase I metabolism, reduction, good for?

A

Low PaO2

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135
Q

Where are drugs that undergo glucuronidation excreted?

A

Bile and urine

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136
Q

What is an example of a condition that interferes with conjugation?

A

Neonatal hyperbilirubinemia

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137
Q

What type of metabolism does not involve CYP enzymes?

A

Hydrolysis

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138
Q

Where does hydrolysis often occur and what type of bond does it usually occur at?

A

Often occurs outside of the liver and at ester bonds

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139
Q

3 examples of drugs that undergo hydrolysis

A
  1. Succinylcholine (Anectin) 2. Esmolol (Brevibloc) 3. Ester Local Anesthetic (Procaine, Cocaine)
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140
Q

What are the Phase II enzymes?

A

“Transferases”

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141
Q

For >50% of anesthetics, what is clearance rate proportional to?

A

Clearance rate is proportional to concentration; More drug/more clearance

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142
Q

Equation for rate of drug metabolism?

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143
Q

What does flow limited metabolism mean?

A

Arterial blood flow, Q, limits metabolic rate

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144
Q

What does capacity limited metabolism mean?

A

Livers ability to metabolize is the limiting factor, SE can build up overtime if re-administration of a drug is too soon

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145
Q

Which drugs, lipid/water soluble, are less likely to be reabsorbed by the kidneys?

A

Water soluble drugs

146
Q

What effect does context sensitive half-time ignore?

A

Plasma-effect site disequilibrium

147
Q

What increases the context sensitive half-time?

A

Longer infusion durations

148
Q

What is an example of a drug class that are weak acids.

A

Barbiturates such as thiopental

149
Q

What are examples of drug classes that would be considered weak bases?

A

Opioids and local anesthetics

150
Q

What form of a drug is lipid soluble, non-ionized or ionized?

A

non-ionized

151
Q

What form of a drug is active, non-ionized or ionized?

A

non-ionized

152
Q

How are non-ionized drugs metabolized?

A

Hepatic metabolism

153
Q

What is the mnemonic to figure out ionization vs non ionization?

A

Weak Acids, PK After pH Weak Bases, PK Before pH Nicely negative numbers are non-ionized

154
Q

What chronic disease would display atypical enzymes?

A

Renal failure

155
Q

3 reasons for varying drug responses in the elderly

A
  1. Decreased cardiac output 2. Decreased protein binding 3. Increased body fat
156
Q

Which enantiomer of ketamine is more potent with less delirium?

A

S-enantiomer

157
Q

Which enantiomer of bupivicaine has 30% less cardiac toxicity?

A

L-Bupivicaine

158
Q

Which isomer of atracurium lacks histamine effects?

A

Cisatracurium (Nimbex)

159
Q

What benefit is there to using Xopenex over albuterol?

A

Xopenex shows no heart rate jump

160
Q

Midazolam (doses)

A

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
Q

Diazepam (doses)

A

Anticonvulsant: 0.1 mg/kg IV Induction: 0.3 - 0.5 mg/kg IV (decrease for elderly/Liver Disease)

162
Q

Lorazepam (doses)

A

1 - 4 mg IV (single dose)

163
Q

Romazicon (doses)

A

0.2 mg IV then 0.1 mg q1min. until desired effect (1 mg max)

164
Q

What are Freud’s three levels of mind?

A
  1. Conscious mind 2. Preconscious mind 3. Unconscious mind
165
Q

What anesthetic drugs were used that showed changes in electrical activity on the EEG?

A

Chloroform and volatile anesthetics

166
Q

What can the EEG be used for in terms of anesthesia?

A

Measure effects

167
Q

What 2 factors related to EEG activity does anesthesia alter?

A

Cerebral blood flow and cerebral metabolic requirement of oxygen

168
Q

What did processing the EEG give us?

A

Bispectral Analysis

169
Q

What did BIS studies show when utilizing hypnotics?

A

BIS change correlated to patient movement

170
Q

What did BIS studies show when utilizing high dose narcotics?

A

Less correlation between BIS and movement

171
Q

At what level of BIS showed that a patient was not conscious?

A

BIS score of <58

172
Q

What did a BIS score of <65 show?

A

Less than 5% chance of return to consciousness within 50 seconds

173
Q

What should the EMG show on a BIS during a procedure?

A

0, if it is above 0 then it indicates lots of patient movement

174
Q

What range of BIS correlates with relatively no recall of the procedure?

A

40-60

175
Q

What would Ketamine give us on a BIS monitor? Beta-blockers?

A

Ketamine - false high Beta blockers - false low

176
Q

When is the best time to give benzodiazepines?

A

Pre-op environment, especially with patients who have chronic anxiety

177
Q

What do benzos cause from the spinal cord?

A

Skeletal muscle relaxation

178
Q

What is the only thing that causes retrograde amnesia?

A

Electroconvulsive therapy

179
Q

What does it mean when we say benzodiazepines cause anterograde amnesia?

A

Patients will not remember anything after the medication has been administered, the amnesic effect will last longer than sedation

180
Q

When metabolizing benzos, what do they lack compare to barbiturates?

A

They do not have hepatic microsomal enzymes

181
Q

Which benzodiazepine has the shortest elimination half time?

A

Midazolam

182
Q

Which benzodiazepines have greater context sensitive half times than midazlolam?

A

Diazepam and Lorazepam, this effect makes them more attractive for sedation postop

183
Q

What is the mechanism of action for benzos?

A

They facilitate GABA agonism, allowing for enhanced opening of Cl- channels

184
Q

What effect does the GABA alpha-1 site have?

A

sedative, amnesic, anticonvulsant

185
Q

Where are the GABA alpha-1 sites found to have effect?

A

cerebral cortex, cerebellar cortex, thalamus

186
Q

What effect does the GABA alpha-2 site have?

A

Anxiolytic, anti-hyperalgesia, skeletal muscle relaxation

187
Q

Where are the GABA alpha-2 sites found to have effect?

A

Hippocampus, amygdala

188
Q

What are 4 other substrates that bind to GABA receptor binding sites and also have a synergistic effect?

A
  1. Barbiturates 2. Etomidate 3. Propofol 4. Alcohol
189
Q

What do benzos bind to in the plasma?

A

Albumin

190
Q

Effects of chronic renal failure/cirrhosis on benzodiazepine metabolism?

A

More free drug, making it more potent

191
Q

What do we tell the patient if we do not administer benzos in the pre-op area?

A

The patient will remember the trip to the OR and going to sleep

192
Q

What effect do benzos have on EEG’s?

A

decrease alpha and fast-beta activity, meaning the EEG is slower

193
Q

Do benzos show tachyphylaxis?

A

Benzos do not show tolerance per EEG

194
Q

What does it mean that benzos do not produce isoelectric states on the EEG?

A

They have a high margin of safety

195
Q

What pathway is Lorazepam (Ativan) metabolized by?

A

Glucuronidation, it does not have any active metabolites and is safer to give the elderly

196
Q

What are the effects of metabolism on Diazepam/Midazolam?

A

Active metabolites

197
Q

What is the risk factor for postoperative confusion when giving benzos?

A

Daily use > 1 year

198
Q

What effect if any do benzos have on platelets?

A

Benzos have been shown in the lab to inhibit platelet aggregating factor

199
Q

3 Important facts about midazolam (versed)

A
  1. Imidazole ring 2. 2-3x as potent as diazepam d/t greater affinity for receptor 3. Amensia > sedation
200
Q

What are the two variations of pH dependent ring opening of midazolam?

A

pH < 3.5, ring opens and is water soluble pH >4.0 ring closes and is lipid soluble

201
Q

What is the onset of action and peak effect time of midazolam?

A

onset of action: 1-2 minutes IV peak effect time: 5 minutes

202
Q

What is the issue with giving midazolam oral?

A

Significant 1st pass effect

203
Q

What is the elimination half time of midazolam?

A

2 hours, this effect is doubled in elderly patients

204
Q

What enzymes metabolize midazolam?

A

CYP3A4

205
Q

What is the active metabolite of midazolam and where is it eliminated through?

A

1-hydroxymidazolam is cleared through the kidneys

206
Q

5 drugs that inhibit CYP40 enzymes

A
  1. Cimetidine 2. Erthromycin 3. CCB 4. Antifungals 5. Fentanyl
207
Q

What effect does not allow midazolam to produce an isoelectric EEG?

A

Ceiling effect

208
Q

What is the effect of midazolam on ICP?

A

No change in ICP, making it good for induction with neuro pathologies

209
Q

What is the effect of midazolam on the pulmonary system?

A

Dose dependent decreases in ventilation, which is exaggerated with opioids/CNS depressant drugs. Midazolam also depresses swallowing reflective and decrease upper airway activity.

210
Q

What is the effect of midazolam on the CV system?

A

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
Q

When and what route do we give midazolam to pedi patients?

A

Oral admin 30 minutes before induction

212
Q

What effect does midazolam have on volatile anesthetics?

A

Dose dependent decreases in volatile requirements

213
Q

What does clearance of midazolam depend on?

A

Hepatic metabolism, the activite metabolites will accumulate and delay awakening

214
Q

What is the recommended time period for post-op sedation with midazolam per the Society of Critical Care Medicine?

A

2-3 days

215
Q

How is the duration of action of diazepam when compared to midazolam?

A

much longer

216
Q

When diazepam is mixed in propylene glycol, what is the side effect?

A

pain on injection/glycol toxicity

217
Q

When diazepam is mixed with soybean formula, what is the side effect?

A

less painful

218
Q

What is the onset of action and elimination half time of diazepam?

A

onset of action: 1-5 minutes elimination half time: 20-40 hours

219
Q

What does diazepam bind to in the plasma?

A

Extensively protein bound

220
Q

How is the duration of action and elimination half time of diazepam when compared to lorazepam?

A

Duration of action is shorter and elimination half time is longer. Diazepam dissociates from GABA faster than lorazepam

221
Q

What pathway does diazepam follow for metabolism?

A

CYP3A

222
Q

What is the active metabolite of diazepam?

A

Desmethyldiazepam and oxazepam

223
Q

When do we se a return of drowsiness with diazepam?

A

6-8 hours

224
Q

Where are the active metabolites of diazepam excreted?

A

in the urine

225
Q

What can diazepam abolish at 0.1mg/kg IV?

A

DT’s, Status epileptics, lidocaine toxicity

226
Q

What benzodiazepine can produce an isoelectric EEG?

A

Diazepam

227
Q

What are the effect of diazepam on ventilation?

A

Minimal effects: 1. Slight decrease Vt 2. After 0.2 mg/kg IV increases in PaCO2 3. Exaggerated with opioids, alcohol, COPD

228
Q

What can reverse the ventilatory depressant effects of diazepam?

A

Surgical stimulation

229
Q

Cardiovascular effects of diazepam?

A

Minimal decreases in BP, CO and SVR with induction doses. BP changes are additive with opioids

230
Q

What benzodiazepine has transient depression of baroreceptor mediated HR response?

A

diazepam

231
Q

What are the neuromuscular effects of diazepam?

A

Skeletal muscle tone decreased through spinal neurons

232
Q

How much do we decrease the dose of diazepam by in the elderly, liver disease patients or in the presence of opioids?

A

25-50% dose reduction

233
Q

What does lorazepam resemble?

A

Oxazepam, it has an extra Cl- atom

234
Q

When compared to midazolam and diazepam, how are the sedative and amnestic effects of lorazepam?

A

more potent

235
Q

What is lorazepam prepared in?

A

Propylene glycol

236
Q

Why does lorazepam have slower entrance to the CNS than midazolam or diazepam?

A

lower lipid solubility

237
Q

What is the peak effect and elimination half time of lorazepam?

A

Peak effect: 20-30 minutes (1-4mg IV) Elimination half time is 14 hours (slower than midazolam)

238
Q

Which benzodiazepine is less affected by hepatic function, age, drugs (cimetidine)?

A

lorazepam

239
Q

What does flumazenil antagonize with the BZD/opioid combo?

A

ventilatory depression

240
Q

What does flumazenil prevent/reverse?

A

All agonist activity of Benzos

241
Q

What is flumazenil a derivative of?

A

1,4 imidazobenzodiazepine

242
Q

What is flumazenil metabolized by?

A

Hepatic microsomal enzymes into inactive metabolites

243
Q

When is flumazenil contraindicated?

A

Use of antiepileptic drugs and predicates acute withdrawal seizures

244
Q

When reversing benzos with flumazenil, will we see acute anxiety, hypertension, tachycardia, or change in MAC?

A

No

245
Q

What did Hippocrates contribute to anesthesia?

A
  1. Accommodate the operator 2. Avoid sinking down and turning away
246
Q

What did Dr. Koller contribute to anesthesia?

A

Utilized cocaine as an anesthetic for eye surgery (Collegague of Sigmund Freud)

247
Q

What did Dr. Halsted contribute to anesthesia?

A

1st regional mandibular nerve block with cocaine

248
Q

What does Histamine induce?

A

endogenous substance involving basophils and mast cells Contraction of SM in airways Acid secretion in the stomach Neurotransmitter release in CNS.

249
Q

H1 Receptors (what do they do when activated)

A

associated with hyperalgesia and inflammatory pain. weak anticholinergic (anti-muscarinic) activity

250
Q

3 things that histamine induces in the body?

A
  1. Contraction of smooth muscles in airway 2. Secretion of acid in the stomach 3. Release of neurotransmitters in CNS
251
Q

2 Process that H1 receptors are involved in

A
  1. Hyperalgesia and inflammatory pain 2. Weak anticholinergic (Anti-muscarinic) activity
252
Q

H1 Receptor Antagonists (Drugs and side effects)

A

Diphenhydramine Promethazine (they are effective AND inexpensive) Side effects include: Blurred vision, urinary retention, dry mouth, drowsiness (1st gen), heart block.

253
Q

What is the greatest side effect from H1 receptor antagonists and why do we see this effect?

A

Sleepiness because they cross the blood brain barrier

254
Q

What are the three MOA’s thought to occur when we give an H1 receptor antagonist?

A
  1. Receptors in vestibular system; effective for motion sickness 2. Allergic Rhinoconjunctivitis 3. Helps w/ anaphylactic reactions
255
Q

H2 Receptors (when activated they…)

A

elevate Cyclic-AMP increase acid production

256
Q

H2 Receptor Antagonists (MOA)

A

decrease gastric volume, but do NOT effect pH

257
Q

Estimated half time and onset of action of Promethazine (Phenergan)?

A

half time: 9-16 hours onset of action: 5 minutes

258
Q

Dose of Promethazine (Phenergan)

A

12.5-25mg

259
Q

What precaution was place on phenergan as a black box warning in 2009?

A

Gangrene if promethazine infiltrated

260
Q

Dose of Promethazine (Phenergan)

A

12.5-25mg

261
Q

Histamine releasing drugs

A

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
Q

Proton Pump Inhibitors (PPIs MOA)

A

irreversibly binds to acid secreting “pumps” stopping the movement of protons across the gastric parietal cells decrease gastric volume AND lower pH

263
Q

PPIs (Drugs and side effects)

A

Omeprazole Pantoprazole Lansoprazole Dexlansoprazole Side effects inlucde: bone fx, Lupus, acute interstitial nephritis, C-Diff, B-12/Mg deficiency, inhibits warfarin metabolism

264
Q

Omeprazole (PPI)

A

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
Q

Omeprazole (side effects)

A

Side effects include: HA, Agitation, confusion, ABD pain, N/V, Flatulence

266
Q

Dose of diphenhydramine?

A

25-50 mg

267
Q

What reflex might be inhibited with diphenhydramine use?

A

Afferent arc of oculo-emetic reflex

268
Q

Does benadryl exacerbate opioid-induced depression of hypoxic response?

A

no

269
Q

Effects of H2 receptor antagonists?

A
  1. Decreased gastric volume 2. No effect on gastric pH
270
Q

4 Side effects of H2 receptor antagonists

A
  1. Diarrhea 2. Headache 3. Skeletal muscle pain if given too quickly 4. Weakend gastric mucosa to bacteria in prolonged administration
271
Q

3 Examples of H2 receptors antagonists

A
  1. Cimetidine (Tagamet) 2. Ranitidine (Zantac) 3. Famotidine (Pepcid)
272
Q

How is cimetidine metabolized and excreted?

A

In the liver by CYP450 and cleared in the urine

273
Q

What effect does cimetidine have on CYP450?

A

Reduces metabolism

274
Q

7 drugs associated with CYP450 metabolism that we don’t want to give concurrently with Tagamet?

A
  1. Warfarin 2. Phenytoin 3. Lidocaine 4. Tricyclics 5. Propranolol 6. Nifedipine 7. Meperidine
275
Q

Adverse effects associated with cimetidine?

A
  1. HA 2. Confusion (Crosses BBB) 3. Bradycardia 4. Hypotension
276
Q

Normal dose of Cimetidine and renal impairment dose?

A

Dose: 150-300 mg IV Renal impairment: 1/2 dose

277
Q

Metabolism and excretion meshing for ranitidine and famotidine?

A

Hepatic metabolism and renal clearance

278
Q

4 known drugs that cause histamine release?

A
  1. Protamine 2. Atracurium 3. Mivacurium 4. Morphine
279
Q

Normal dose and renal impairment dose for ranitidine?

A

Normal: 50mg diluted to 20CC over 2 min Renal impairment: 1/2 dose

280
Q

Which H2 receptor antagonist has no effect on CYP enzymes?

A

Famotidine (Pepcid)

281
Q

Normal dose and renal impairment dose for famotidine (Pepcid)?

A

Normal: 20mg IV Renal impairment: 1/2 dose

282
Q

What are proton pump inhibitors most effective for treating?

A
  1. Controlling gastric acidity 2. Decreasing gastric volume
283
Q

Which Histamine receptor antagonist, if given alone in anaphylaxis, has been shown to worse symptoms?

A

H2

284
Q

6 pathologies that PPI’s have been associated with?

A
  1. Bone fractures 2. SLE 3. Acute intestinal nephritis 4.. C-diff 5. Vitamin B12/Magnesium Deficiency 6. Inhibits warfarin metabolism
285
Q

What are proton pump inhibitors most effective for treating?

A
  1. Controlling gastric acidity 2. Decreasing gastric volume
286
Q

3 actions of omeprazole

A
  1. Released in small intestine (prodrug) 2. Returns to parietal cells 3. Acid-inhibition increases with repeated dosing
287
Q

6 pathologies that PPI’s have been associated with?

A
  1. Bone fractures 2. SLE 3. Acute intestinal nephritis 4.. C-diff 5. Vitamin B12/Magnesium Deficiency 6. Inhibits warfarin metabolism
288
Q

4 examples of PPIs

A
  1. Omeprazole (Prilosec) 2. Pantoprazole (Protonix) 3. Lansoprazole (Prevacid) 4. Dexlansoprazole (Dexilent)
289
Q

When do we significantly greater control with prilosec administration?

A

Daytime, nocturnal and meal acid secretion more so than h2 drugs

290
Q

What is omeprazole (Prilosec) metabolized by?

A

CYP enzymes, but causes no clinically significant inhibition of other drugs

291
Q

Dose of omeprazole?

A

40 mg in 100 cc NS over 30 minutes or PO >3 hours prior

292
Q

SE associated with omeprazole?

A
  1. HA 2. Agitation 3. Confusion 4. ABDOMINAL PAIN 5. N/V 6. Flatulence
293
Q

What is pantoprazole (protonix) metabolized by?

A

CYP enzymes in the liver

294
Q

What H2 receptor antagonist does protonix work just as fast as?

A

Ranitidine (Zantac)

295
Q

How long prior to surgery should we give pantoprazole to see a decrease in gastric volume and pH

A

1 hour prior

296
Q

Dose of pantoprazoe (protonix)

A

40 mg in 100 mL over 2-15 minutes

297
Q

Treatment of choice for GERD?

A

PPI (increased pH and decreased gastric volume)

298
Q

Treatment of choice for gastroduodenal ulcers?

A

PPI

299
Q

Treatment of choice for aspiration pneumonitis?

A

H2 blockers b/c they work faster

300
Q

Treatment of choice for acute upper GI bleed?

A

PPI infusion post EGD tx

301
Q

Treatment of choice for aspiration pneumonitis?

A

H2 blockers b/c they work faster

302
Q

Promethazine (H1 receptor antagonist)

A

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
Q

What is an example of an antacid?

A

Sodium citrate (Bicitra)

304
Q

What are the two side effects seen from long term antacid us?

A
  1. Acid breakdown of food inhibited 2. Acid rebound can occur
305
Q

3 side effects associated with magnesium based antacids?

A
  1. Osmotic diarrhea 2. Neurologic impairment 3. Neuromuscular impairment (diminished deep tendon reflexes)
306
Q

3 side effects associated with calcium based antacids?

A
  1. Hypercalcemia 2. Kidney stones 3. Dysrythmias
307
Q

Non-particulate antacids neutralize acid, what cases are these good for?

A
  1. Trauma 2. Obese patients with reflux 3. Emergent c-sections
308
Q

2 effects seen when using Sodium Citrate (Bicitra)

A
  1. Protection against aspiration pneumonia 2. Increases intra-gastric volume up to 30cc
309
Q

What are the two effects seen from long term antacid us?

A
  1. Acid breakdown of food inhibited 2. Acid rebound can occur
310
Q

3 effects associated with magnesium based antacids?

A
  1. Osmotic diarrhea 2. Neurologic impairment 3. Neuromuscular impairment (diminished deep tendon reflexes)
311
Q

3 Patient populations that we assume have a full stomach?

A
  1. Insulin dependent diabetics d/t delayed gastric motiity 2. Trauma patients 3. Pregnant women >12 weeks gestation
312
Q

Effect associated with Sodium based antacids?

A

Increased sodium load

313
Q

Dose and Onset of action of sodium citrate?

A

dose: 15-30 mL PO onset of action: Immediately

314
Q

When do you lose effectiveness of sodium citrate?

A

30-60 minutes after administration

315
Q

What major reaction do we see with administration of metoclopromide (raglan) and how do we dampen this?

A

Extrapyramidal reactions d/t crossing the BBB and we can dampen by given benadryl first

316
Q

What is the only drug cleared by the FDA for diabetics gastroparesis?

A

Reglan

317
Q

3 examples of dopamine blockers?

A
  1. Metocolopramide (Reglan) 2. Domperidone [Associated with cardiac arrest) 3. Droperidol (Inapsine)
318
Q

SE associated with reglan?

A
  1. Abdominal cramping (if rapid IV admin) 2. Hypotension and HR changes 3. Extra pyramidal symptoms and increased sedation with CNS deppressants
319
Q

Dose of metoclopramide and when to administer it?

A

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

320
Q

Why is domperidone not FDA approved?

A

It is associated with Dysrhythmias and sudden death

321
Q

What does domperidone increase the secretion of?

A

Prolactin secretion by pituitary gland

322
Q

Why is domperidone not FDA approved?

A

It is associated with Dysrhythmias and sudden death

323
Q

H2 Receptor Antagonists (MOA)

A

decrease gastric volume, but do NOT effect pH

324
Q

What two diagnosis was droperidol (inapsine) developed to treat?

A
  1. Schizophrenia 2. Psychosis
325
Q

What is the blackbox warning associated with droperidol?

A

QT prolongation with higher doses such as 2.5-5mg IV

326
Q

Dose of droperidol (Inapsine)

A

0.625-1.25mg IV

327
Q

Where is serotonin released from in the small intestine?

A

Chromaffin cells

328
Q

Where are the 5HT3 receptors found?

A

Kidneys, colon, liver, lung, stomach

329
Q

Where are high concentration of 5HT3 receptors found that are linked to vomiting?

A

Brain and GI tract

330
Q

5HT3 antagonists have almost no side effects, were great for PONV and were originally use in the treatment of what?

A

Chemotherapy and Radiation therapy related N/V (CIV)

331
Q

What are 5HT3 receptor antagonist NOT effective in treating?

A

motion sickness/vestibular stimulation

332
Q

3 Examples of 5HT3 receptor antagonist?

A
  1. Ondansetron (Zofran) [Works the best] 2. Granisetron (Kytril) 3. Dolasteron (Anzemet)
333
Q

Which 5HT3 antagonist was the first of its kind and does not have an CNS effects?

A

Ondansetron (Zofran)

334
Q

Dose and plasma half life of ondansetron (zofran)?

A

Dose: 4-8mg IV Plasma 1/2: 4 hours

335
Q

What are three possible MOA’s of corticosteroids?

A
  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
Q

What receptor is droperidol (inapsine) a strong antagonists of?

A

D2 receptors

337
Q

What annoying side effect is associated with dexamethasone admin?

A

perineal burning/itching

338
Q

What is the dose if corticosteroids are used for PONV?

A

4-8 mg IV

339
Q

What is the delay in onset of dexamethasone (decahedron) and how long does its efficacy persist?

A

Delay in onset of 2 hours and efficacy persists for 24 hours

340
Q

What annoying side effect is associated with dexamethasone admin?

A

perineal burning/itching

341
Q

What class of drug is scopolamine?

A

Competitive muscarinic antagonist

342
Q

Where is the thinnest area available for a scopolamine patch?

A

Post auricular area (behind the ear)

343
Q

Priming dose of scopolamine?

A

1.5mg @ 5mcg/hour

344
Q

SE associated with scopolamine patches?

A

Dilated pupils and light sensitivity

345
Q

How long does 1 scopolamine patch last?

A

24-72 hours

346
Q

Priming dose of scopolamine?

A

1.5mg @ 5mcg/hour

347
Q

What 3 effects are seen cellularly when giving bronchodilators?

A
  1. Activate cAMP 2. Decrease Calcium ion entry 3. Decrease contractile protein sensitivity to Calcium ions
348
Q

Which version of bronchodilators is more lipophilic? SABA or LABA?

A

LABA (long acting bronchodilator)

349
Q

What is the advantage of using levo-albuterol (xopenex) over albuterol (proventil)?

A

Xopenex does not see as big of a jump in HR

350
Q

H2 Receptor Antagonists (Drugs and Side Effects)

A

Cimetidine Ranitidine Famotidine Side effects include: Diarrhea, HA, Skeletal muscle pain, Weakened gastric mucosa to bacteria (prolonged use)

351
Q

Cimetidine (H2 receptor antagonist)

A

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
Q

Ranitidine (H2 receptor antagonist)

A

hepatic metabolized, urine cleared (moderate CYP450 binding) Dose: 50 mg diluted to 20 ml over 2 minutes (half for renal disease)

353
Q

Famotidine (H2 receptor antagonist)

A

hepatic metabolism, urine cleared (none/least CYP450 binding) Dose: 20 mg IV (half for renal disease)

354
Q

Histamine releasing drugs

A

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
Q

Proton Pump Inhibitors (PPIs MOA)

A

irreversibly binds to acid secreting “pumps” stopping the movement of protons across the gastric parietal cells decrease gastric volume AND increases pH

356
Q

PPIs (Drugs and side effects)

A

Omeprazole Pantoprazole Lansoprazole Dexlansoprazole Side effects inlucde: bone fx, Lupus, acute interstitial nephritis, C-Diff, B-12/Mg deficiency, inhibits warfarin metabolism

357
Q

Omeprazole (PPI)

A

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
Q

Omeprazole (side effects)

A

Side effects include: HA, Agitation, confusion, ABD pain, N/V, Flatulence

359
Q

Pantoprazole (PPI)

A

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
Q

Induction of anesthesia drugs

A

Etomidate, ketamine, propofol, narcotics

Advanced Pharmacology 2 (5 decks)

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