Chapters 19, 23, 24 (Learning Outcomes) Flashcards

1
Q

What is the effect of anesthesia?

A

Loss of feeling or sensation

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2
Q

What is general anesthesia categorized by?

A
  1. State of unconsciousness
  2. Analgesia
  3. Amnesia
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3
Q

What is regional anesthesia?

A

When sensory transmission from a specific area/region of the body to the CNS is blocked

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4
Q

What is the effect of neuromuscular blocking agents?

A

Cause muscle paralysis (loss of motor function)

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5
Q

What two groups can neuromuscular blocking agents be broken down into?

A
  1. Depolarizing

2. Non-depolarizing

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6
Q

What is the prototype drug for inhaled anesthetics?

A

Isoflurane (Forane)

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7
Q

What is the prototype drug for regional anesthetics?

A

Lidocaine (Xylocaine)

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8
Q

What are the prototype drugs for neuromuscular blocking agents?

A
  1. Depolarizing = Succinylcholine

2. Non-depolarizing = Vecuronium

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9
Q

At the synaptic level, what is the action of anesthetics?

A

May provoke a decreased release of neurotransmitters or an increased re-uptake and inhibition of postsynapthic enzymes

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10
Q

How does local anesthesia act to stop nerve transmission?

A

Reversibly block all nerve impulses by disrupting membrane permeability to sodium during an action potential
- therefore stop the generation and propagation of the nerve impulse

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11
Q

Describe how Non-depolarizing drugs cause paralysis.

A

They are competitive antagonists that prevent the binding of Ach to the receptor, therefore, the end plate is unable to depolarize

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12
Q

Describe how depolarizing drugs cause paralysis.

A

Structurally similar to Ach, and cause continuous muscle depolarizing and prevent repolarization
- muscle is unable to repolarize as long as the drug continues to bind to the Ach receptor

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13
Q

What are the four LEVELS of sedation?

A
  1. Minimal sedation
  2. Moderate sedation and analgesia (conscious sedation)
  3. Deep sedation and analgesia
  4. Anesthesia
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14
Q

What are the four STAGES of anesthesia?

A

Stage 1 = analgesia
Stage 2 = Delirium/excitment
Stage 3 = Surgical Anesthesia
Stage 4 = Meduallary depression

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15
Q

What is occurring during Stage 1 analgesia?

A

Duration is from start of anesthesia to the loss of consciousness

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16
Q

What happens during Stage 2 (delirium/excitment)?

A
  • systolic blood pressure rises
  • may experience excitation, agitation, restlessness
  • increased RR
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17
Q

What happens during Stage 3 (surgical anesthesia)?

A
  • Begins with resumption of regular respiration
  • beginning of muscle relaxation
  • By plane IV, spontaneous respiration ceases
    (there are four planes to stage 3)
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18
Q

What happens during Stage 4 (medullary depression)?

A

Respiratory and vasomotor centers are depressed

  • spontaneous respiration has ceased
  • marked hypotension with weak and irregular pulse
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19
Q

What are general anesthetics used for?

A

To induce and maintain anesthesia during surgery

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20
Q

What is Isoflurane used for?

A

To induce and maintain anesthesia

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21
Q

Describe the pharmacokinetics of isoflurane

A

Administered: Inhalation
Metabolism: 0.2% is taken up
Excreted: pulmonary
Onset: secs to mins

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22
Q

Describe the pharmacodynamics of Isoflurane

A

Exact mechanism is unknown

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23
Q

How can we minimize the adverse effects of Isoflurane?

A

Monitor blood pressure and temperature to detect residual hypotension

  • possibility of malignant hyperthermia
  • manage shivering and tremors
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24
Q

What happens when Isoflurane is mixed with a non-depolarizing muscle agent?

A

Prolongs the blockage and potentiates the effects

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25
Q

What is the most serious adverse effect of Isoflurane?

A

Respiratory depression

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26
Q

What are intravenous (IV) anesthetics also known as?

A

Induction agents

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27
Q

What class of IV anesthetic agents does Propofol fall into?

A

Non-barbiturate hypnotic agent

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28
Q

What are the 4 classess of intravenous anesthetic agents?

A
  1. Barbiturates
  2. Benzodiazepines
  3. Opiod analgesics
  4. Nonbarbiurate hypnotic agents
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29
Q

What is Propofol (Diprivan) used for?

A

Induction and maintenance of general anesthesia

- and maintenance of sedation in the ICU

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30
Q

Describe the pharmacokinetics of Propofol

A

Administered: Intravenously
Onset: 40 secs
Dur: 3 to 5 minutes
Metabolized: Hepatic and lung routes

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31
Q

What is the advantage of Propofol?

A

The rapid return of consciousness with minial psychomotor impairment

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32
Q

Describe the pharmacodynamics of Propofol

A

Cellular mechanism action is unknown

- thought to mediate activity of the inhibitory GABA receptors

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33
Q

What are three example of benzodiazepines?

A
  1. Diazepam
  2. Lorazepam
  3. Midazolam
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34
Q

What is Fentanyl?

A

Opioid analgesic

- used in general anesthesia and conscious sedation

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35
Q

What do you need to be aware of prior to administering Fentanyl?

A

Respiratory rate

- causes respiratory depression

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36
Q

How are local anesthetics divided into two classes? What are they?

A

Based on their chemical structure

  1. Esters
  2. Amides
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37
Q

How do local anesthetics produce local or regional anesthesia and analgesia?

A

By blocking electrical transmission of pain along nerve fibers and abolishing sensations in a limited and well-defined area of the body
- without loss of consciousness

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38
Q

What nerve function is affected first when local anesthetic is applied?

A
  1. Temperature
  2. Pain
  3. Touch
  4. Proprioception
  5. Skeletal muscle tone
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39
Q

What is the prototype drug of local anesthetics?

A

Lidocaine (Xylocaine)

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40
Q

When is lidocaine used?

A
  • Regional blocks
  • Peripheral nerve blocks
  • Ophthalmic anesthesia
  • Dental anesthesia
  • Infiltration anesthesia
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41
Q

What addition can prolong the effect of Lidocaine?

A

Epinephrine slows the vascular absorption and prolongs its effects

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42
Q

True or False:

Lidocaine is susceptible to the first pass effect of the liver

A

True!

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43
Q

Describe the pharmacodynamics of Liodcaine

A

Produces its analgesic effects through a reversible nerve conduction blockade
- decreases the rate of membrane depolarization

44
Q

In both depolarizing and non-depolarizing agents, where does the neuromuscular block occur?

A

At Ach receptor sites on the motor end plate

45
Q

What is the prototype drug of Non-depolarizing neuromusclar blocking agent?

A

Vecuronium (Norcuron)

46
Q

Describe the pharmacotherapeutics of Vecuronium

A

A non-depolarizing muscle relaxant

- used to provide skeletal muscle relaxation to facilitate intubation and mechanical ventilation

47
Q

What route is Vecuronium available in?

A

IV use only

48
Q

Describe the pharmacodynamics of Vecuronium

A
  • anatgonists of Ach, compete with the neurotransmitter for the cholinergic receptor sites at the motor end plate
49
Q

What is important to keep in mind if there is prolonged paralysis due to Vecuronium?

A

Change the patients position frequently to prevent venous stasis

50
Q

How do depolarizing NMJ blockers work?

A

By causing the muscle cell membrane to depolarize or become excited
- causes muscle contraction

51
Q

What is the prototype drug for depolarizing NMJ blockers?

A

Succinylcholine (Anectine)

52
Q

What is succinylcholine primarily used for?

A

Rapid endotracheal intubation

- very short-acting paralytic

53
Q

Describe the pharmacodynamics of Succinylcholine

A

Acts as an agonist at the cholinergic nicotinic receptors of the motor end plate

  • depolarizes the postsynaptic membrane
  • producing repetitive excitation of the motor end plate
54
Q

What do patients commonly experience after receiving succinylcholine?

A

Muscle pain

- from rapid contraction followed by flaccid paralysis

55
Q

What are the three types of drugs used to treat pain?

A
  1. Strong narcotics
  2. Mild narcotics
  3. Mixed agonist-antagonists
56
Q

What is the prototype for strong narcotics?

A

Morphine

57
Q

What is the prototype for mild narcotics?

A

Codeine

58
Q

What is the prototype drug for mixed agonist-antagonist opioid?

A

Pentazocine

59
Q

What is transduction?

A

Term used to describe the phenomena associated with the initiation of a pain signal

60
Q

What do afferent nerves carry signals to?

A

To the CNS

61
Q

What do efferent nerves carry signals to?

A

To the peripheral

62
Q

What is nociceptic pain caused by?

A

Injury, disease or inflammation

- indicates real or potential tissue damage

63
Q

How can nociceptic pain be categorized as?

A

Somatic

Visceral

64
Q

What does somatic pain result from?

A

Ongoing activation of peripheral nociceptors found in bone, muscle or soft tissue

65
Q

What does visceral pain result from?

A

Stimulation within the deep tissues or organs and surrounding structural tissues

66
Q

What is neuropathic pain used to describe?

A

Pain in which the underlying pathology is abnormal processing of stimuli in the peripheral or CNS

67
Q

What is acute pain?

A

Immediate phase of response to an insult or injury

68
Q

How is chronic pain resolved?

A

With the healing of the underlying injury

69
Q

What is chronic pain?

A

Pain that persists well beyond actual tissue injury and healing

70
Q

What is easier to do, decrease pain or prevent pain?

A

Prevent pain

71
Q

What are the two drug classifications that are normally used for pain management?

A
  1. Opioid analgesics

2. Non-steroidal anti-inflammatory (NSAIDs)

72
Q

What are narcotics?

A

Opioids

73
Q

What is the action on NSAIDS?

A

Work on the peripheral nervous system, preventing the transmission of the pain nerve impulse

74
Q

What are adjunct analegsics?

A

Drugs that are used secondarily for pain relief

  • anti-depressants
  • corticosteriods
  • antiepileptics
75
Q

List the following drugs in order of strength: Morphine, Hydromorphone, Oxycodone, Fentanyl

A
  1. Fentanyl
  2. Hydromorphone
  3. Oxycodone
  4. Morphine
76
Q

What is the prototype drug of a strong narcotic agonist?

A

Morphine

77
Q

What is the drug that is the narcotic antagonist?

A

Naloxone

78
Q

What does Morphine cause?

A

Respiratory depression

79
Q

What are some examples of secondary pharamacologic actions of morphine (and other narcotics)?

A
  • Respiratory depression
  • Hypotension
  • Euphoria
  • N/V
  • Itching, flushing, red eyes
  • Abdominal pain/cramps
  • Constipation
  • Urinary retention
80
Q

How can a morphine overdose be treated?

A

Naloxone (Narcan)

81
Q

What should be assessed prior to administering Morphine?

A
  • RR
  • cardiac, renal, hepatic, pulmonary disease
  • hypothyroidism
  • addison disease
  • prostatic hypertrophy
82
Q

Define tolerance

A

Body has become accustomed to the effects of a substance

- patient must use more to achieve desired effect

83
Q

Define physical dependence

A

A withdrawal when Morphine is discontinued

- an exaggerated rebound from its acute effects

84
Q

Define addiction

A

Compulsive use of the drug for a secondary gain, not for pain control

85
Q

What is breakthrough pain?

A

Transitory flare-ups of pain over baseline in a patient receiving opioid therapy

86
Q

What is incidental pain?

A

Spontaneous or activity-related pain

- may be specific movement or all movements

87
Q

What is the prototype for mild narcotic agonists?

A

Codeine

88
Q

What does codeine do to your cough?

A

It suppresses it

89
Q

How are fever, inflammation and pain commonly controlled by?

A

Salicylates
NSAIDs
Para-aminophenol derivative drugs

90
Q

How are migraine headaches typically treated?

A

With Triptans

91
Q

What fever-inducing substance causes fever?

A

Pyrogens

92
Q

What are the classic signs of the inflammatory response?

A
Redness
Warmth
Swelling
Pain
Loss of function
93
Q

What are salicylates used for?

A

Conditions ranging from simple headache to acute MI

94
Q

What are NSAIDs primarily used for?

A

Anti-inflammatory drugs

- also analgesics

95
Q

What is the prototype drug for salicylates?

A

Acetylsalicylic acid (Aspirin)

96
Q

Other than pain reduction and inflammation, what is another use of Aspirin?

A

Antiplatelet

- helps to prevent transient ischemic attacks, MIs, and stokes

97
Q

When is aspirin contraindicated?

A

Bleeding disorders

- anticoagulation

98
Q

What are two adverse effects of aspirin therapy?

A
  1. Salicylism (mild aspirin toxicity)

2. Salicylate poisoning (life-threatening)

99
Q

What are the most serious adverse effects of aspirin?

A
  • renal impairment
  • gastric ulceration
  • GI bleeding
100
Q

What is the prototype drug for NSAIDs?

A

Ibuprofen (Motrin, Advil)

101
Q

What are the labeled uses of Ibuprofen?

A
  • RA
  • OA
  • Mild to moderate pain
  • Migraine headache
  • Fever
  • Menstrual cramps
102
Q

What can chronic use of Ibuprofen result in?

A
  • Gastritis
  • Ulceration
  • GI bleeding
103
Q

How can you maximize the therapeutic effects of Aspirin?

A

Give with milk or food to decrease gastric distress

104
Q

What is the only para-aminophenol derivative that is available in the US?

A

Acetaminophen (Tylenol)

105
Q

What is oral acetaminophen indicated for treating?

A

Fever and mild pain

106
Q

What is the maximum recommended dose in a 24 period for Tylenol?

A

4 grams

107
Q

How does Acetaminophen’s antipyretic action work?

A

Results from inhibiting prostaglandin synthesis in the CNS