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PT 2 > Block 7 - L1-L4 > Flashcards

Block 7 - L1-L4 Flashcards

1
Q

What are the endogenous opioid peptide families implicated in acupuncture analgesia?

A
  1. Beta-endorphin
  2. Enkephalin
  3. Dynorphin
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2
Q

What are the major NT implicated in acupuncture analgesia?

A
  1. 5-HT
  2. NE
  3. Substance P
  4. GABA
  5. Dopamine
  6. ACTH
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3
Q

List the various afferent nerve fibers involved in transmitting pain impulses.

A
  1. C fibers (large unmyelinated)

2. A-delta fibers (small myelinated)

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4
Q

Describe transmission of a painful stimulus.

A
  1. An injury to the skin activates the sensory receptors of small afferent A-delta and C-fibers.
  2. These synapse onto the STT in the SC.
  3. The STT projects to the thalamus.
  4. The thalamus projects to the primary sensory cortex.
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5
Q

What does low frequency/high intensity PENS mean? High frequency/low intensity?

A

2 to 15 Hz as strong as the patient can tolerate

30 to 200 Hz just to where the patient can barely feel it

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6
Q

Describe the effect of low frequency/high intensity electro-acupuncture stimulation.

A
  1. Needle activates a Type II or III small afferent nerve from a sensory receptor in the muscle.
  2. This cell synapses in the SC onto an anterolateral tract (ALT) cell.
  3. This projects to the SC, midbrain, and pituitary-hypothalamus complex.
  4. In the SC, the ALT tract causes release of enkephalin or dynorphin pre-synaptically. This inhibits transmission of pain pre-synaptically in the SC.
  5. In the midbrain, cells in the periaqueductal gray are excited. This causes release of enkephalin, which disinhibits another cell. This activates the raphe nucleus in the medulla, causing it to send impulses down the dorsolateral tract. This releases monoamines (5-HT, NE) onto SC cells. This causes post-synaptic inhibition of pain.
  6. In the pituitary/hypothalamus, beta-endorphin and ACTH are released.
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7
Q

Describe the effect of high frequency/low intensity electro-acupuncture stimulation.

A

This only stimulates the spinal cord and midbrain. Specifically, the SC releases GABA post-synaptically.

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8
Q

Why are needles also placed at distal points (away from the painful region)?

A

To activate the midbrain and hypothalamic-pituitary complexes - causes endorphin release

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9
Q

Compare low frequency/high intensity to high frequency/low intensity as it relates to the substances released and the locations of this release.

A

LF/HI:
SC: enkephalin, dynorphin B
Midbrain: enkephalin, serotonin, NE
Pituitary/hypothalamus: B-endorphin, ACTH

vs.

HF/LI:
SC/midbrain only: GABA

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10
Q

Compare low frequency/high intensity to high frequency/low intensity as it relates to the effect of naloxone.

A

LF/HI: effect blocked by naloxone

vs.

HF/LI: effect not blocked by naloxone

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11
Q

Compare low frequency/high intensity to high frequency/low intensity as it relates to the results.

A

LF/HI: slow onset, long duration, cumulative effects

vs.

HF/LI: fast onset, short duration, non-cumulative effects

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12
Q

What is the thermocouple effect of Kelvin-Thomas?

A

A gradient along the length of a homogenous conductor with a temperature gradient produced by the ends of the conductor at different temperatures

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13
Q

What is the Benedick’s effect?

A

The current along a uniform conductor is reinforced by the electro-magnetic effect between the second (spiraled) metal of the handle in contact with the first metal of the shaft.

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14
Q

What are the some of the recommended uses for acupuncture as described by the NIH consensus panel?

A

Adult post-operative and chemotherapy nausea and vomiting and in postoperative dental pain

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15
Q

From what plant are exogenous opioids harvested?

A

Poppies (papaver somniferum and papaver album)

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16
Q

What is any substance, natural or synthetic, that produces morphine-like effects that are blocked by antagonists such as naloxone?

A

Opioid

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17
Q

What are compounds that are found in the opium poppy?

A

Opiate

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18
Q

What is a narcotic?

A

Something that induces sleep

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19
Q

What are the 6 therapeutic uses of opioids?

A
  1. Pain management
  2. Anesthesia, sedation
  3. Anti-diarrheal
  4. Antitussive
  5. Treatment of dyspnea
  6. Treatment of addiction
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20
Q

What are the corresponding pharmacological effects of opioids for each therapeutic use?

A
  1. Analgesia (pain management)
  2. Sedation (anesthesia)
  3. Decreased tone in intestinal muscle and decreased secretions (anti-diarrheal)
  4. Depression of cough reflex (antitussive)
  5. Respiratory depression (treatment of dyspnea)
  6. Addiction, dependence, euphoria (treatment of addiction)
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21
Q

What are the risks and AE of opioids?

A
  1. Addiction, abuse, OD
  2. Tolerance
  3. Physical dependence (withdrawal symptoms if stopped)
  4. Increased pain sensitivity
  5. GI - constipation, N/V, dry mouth
  6. CNS - sleepiness, dizziness, depression, confusion
  7. Sexual - decreased testosterone, decreased sex drive/energy/strength
    8 Derm - pruritis, sweating
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22
Q

What are the features o the opioid receptors?

A
  1. 7 transmembrane domains
  2. Membrane bound
  3. G-protein coupled
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23
Q

How does opioid receptor activation block pain pathways pre-synaptically?

A

Stimulation of mu opioid receptors leads to inhibition of AC, which prevents opening of calcium channels, reducing NT release

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24
Q

How does opioid receptor activation block pain pathways post-synaptically?

A

Stimulation of mu opioid receptors increases potassium channel opening, causing hyperpolarization and stimulating the MAPK cascade

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25
Q

List the sites where opioids activate opioid receptors to relieve pain.

A
  1. Receptors in the periphery block nociceptor activation
  2. Receptors on second-order pain transmission neurons block ascending STT to medulla
  3. Receptors at C-fiber terminals in SC blocks release of pain NT
  4. Receptors in the midbrain activate descending systems in PAG mediated by NE and 5-HT
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26
Q

How do opioids induce respiratory depression?

A

Opioids alter the response of the body to arterial CO2 levels at the ventilatory control center in the medulla. Normally, minute volume should increase with rising levels. Opioids produce a blunted response of minute volume. This can lead to brain injury and death.

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27
Q

What structural feature of morphine and derivative drugs gives it the opioid activity?

A

Free -OH on a benze ring linked by 2 C atoms to N atom

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28
Q

Which opioid receptor agonists are most clinically useful and why?

A

Those with a high affinity for mu receptors (morphine, fentanyl, levorphanol, methadone, sufentanil, etc.)

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29
Q

What are the effects of opioid receptor agonists at mu receptors?

A
  1. Analgesia (supraspinal - mu1, spinal - mu2)
  2. Respiratory depression (mu2)
  3. Euphoria
  4. Miosis
  5. Physical dependence
  6. Sedation
  7. Inhibition of GI motility
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30
Q

What are the effects of opioid receptor agonists at delta receptors?

A
  1. Analgesia (spinal)
  2. Respiratory depression
  3. Inhibition of GI motility
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31
Q

What are the effects of opioid receptor agonists at kappa receptors?

A
  1. Analgesia (spinal, peripheral)
  2. DYSPHORIA
  3. Miosis
  4. Sedation
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32
Q

How is heroin different than moprhine?

A

Heroin is more lipid soluble (acetyl groups) than morphine, so it passes the BBB more efficiently.

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33
Q

What are the indications for moprhine?

A
  1. Analgesia
  2. Dyspnea
  3. Anti-diarrheal (in suspension with kaolin)
  4. Antitussive
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34
Q

How is morphine metabolized?

A

Conjugation with glucuronic acid

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35
Q

What causes the analgesic effect of morphine?

A

Morphine-6-glucuronide

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36
Q

How is morphine-6-glucuronide excreted?

A

Via the kidney (caution in renal failure, children, elderly)

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37
Q

How is codeine different from morphine?

A

Greater oral efficacy
Lower first-pass metabolism
Metabolized by liver
Low opioid receptor affinity

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38
Q

What is the indication for codeine?

A

Anti-tussive

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39
Q

What are the indications of the D-isomer of Levorphanol (destrometorphan)?

A

Antitussive

Not analgesic, NMDA receptor inhibition

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40
Q

The L-isomer of Levorphanol (Levo-Dromoran) binds ___ receptors. It can be administered ___. It is similar to morphine - how is it different?

A

Receptors: mu, kappa, and delta
Administration: IV, IM, PO
Less N/V, longer half life, repeated administration leads to accumulation in the plasma

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41
Q

What are the CNS effects of meperidine on the CNS?

A
  1. Strong analgesic
  2. Pupillary constriction, sensitivity of labyrinthine apparatus
  3. Decreased secretion of pituitary hormones
  4. CNS excitation, tremors, seizures
  5. Local anesthetic effects
  6. Respiratory depression
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42
Q

What are the cardiovascular effects of meperidine?

A

Increase in HR (after IV due to release of histamine; not for IM)

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43
Q

What are the smooth muscle/GI tract effects of meperidine? How does this compare with morphine?

A

Slows gastric emptying, delays absorption of other drugs

Less constipation and more CNS bioavailability than morphine

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44
Q

What are the indications for meperidine?

A
  1. Analgesia
  2. Treatment of drug-induced rigors and shaking chills
  3. Diarrhea
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45
Q

What drugs can induce rigors and shaking chills?

A

IV amphotericin B, aldesleukin, trastuzumab, alemtuzumab

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46
Q

Meperidine congeners are used as a ___ drug.

A

Anti-diarrheal

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47
Q

What synthetic opioids are used in anesthesia?

A

Fentanyl, sufentanil, remifentanil, and alfentanil

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48
Q

What are the benefits to using opioids in anesthesia?

A
  1. Short time to peak analgesic effect
  2. Rapid termination of effect after small bolus doses
  3. Cardiovascular safety
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49
Q

What are fentanyl and derivatives indicated for?

A
  1. Anesthetic adjuvants

2. Chronic pain treatment

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50
Q

What is tramadol?

A

Synthetic codeine analog and weak mu agonist

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51
Q

What is a significant AE of Tramadol?

A

Seizures

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52
Q

What are the AE of pentazocine, butorphanol, and nalbuphine?

A

Dysphoria and psychotomimetic effects, increased BP and HR

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53
Q

What are the major contraindications of opioids?

A
  1. Increased sensitivity (neonates, compromised BBB, elderly)
  2. Hepatic or renal disease
  3. Compromised respiratory function
  4. Patients with head injury or elevated ICP
  5. Patients with reduced blood volume or hypotension
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54
Q

What gives morphine derivatives anatagonist activity?

A

Bulky substituent on the nitrogen atom of moprhine

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55
Q

What are the major opioid receptor antagnoists?

A

Naloxone, Naltrexone, Buprenorphine

56
Q

What are the indications for opioid receptor antagonists?

A
  1. Opioid overdose (reversal by naloxone)
  2. Constipation (methylnaltrexone)
  3. Management of abuse syndromes
57
Q

What are cautions related to opioids and analgesia?

A
  1. Opioids are not first line therapy for pain

2. Establish goals for pain management

58
Q

What are some of the goals of anesthesia?

A

Unconsciousness, amnesia, immobility, prevent post-operative N/V, retention or improvement of pre-operative organ systemic functions

59
Q

What is the Meyer-Overton hypothesis of inhalational anesthetics?

A

The higher the lipid solubility of the drug, the more potent it is

60
Q

What might be the MOA of inhalational anesthetics?

A

GABA chloride channel IPSP (hyperpolarization)

61
Q

True or false - there is no antidote for inhalational anesthetics.

A

True

62
Q

What are the stages of general anesthesia?

A
  1. Pre-operative anxiolytic +/- analgesic
  2. Pre-oxygenation (de-nitrogenation)
  3. Induction
  4. Maintenance
  5. Emergence (turn off the gas, give 100% oxygen, breathe, extubate)
  6. Recovery
63
Q

What is the minimum alveolar concentration (MAC)?

A

The minimum alveolar concentration at 1 ATM that prevents movement during a skin incision in 50% of people

64
Q

What influences MAC?

A

Temperature, age, and other medications (not influenced by sex, oxygen, pH, BP)

65
Q

What is the relationship between cardiac output and induction of inhalational anesthetics?

A

As CO increases, induction takes longer (is slower)

66
Q

What is the path of inhalational anesthetics through the body?

A

Machine - alveoli - arterial blood - brain - venous blood - alveoli - machine

67
Q

How do we measure the amount of inhalational anesthetic going to the brain?

A

Fa/Fi = end-tidal/inspired = amount returned to alveoli/amount delivered

68
Q

Describe the concept of cascade.

A

The faster the agent gets from one compartment (airway, alveoli, blood, brain) to the next, the slower it reaches equilibrium

69
Q

How can uptake and distribution of the inhalational anesthetic be increased?

A

Increase delivery to increase speed of induction, increase [agent], increase MV

70
Q

After delivery to the alveoli, what three factors determine uptake into the blood?

A
  1. Solubility
  2. Partial pressure difference
  3. Cardiac output
71
Q

Discuss the solubility of NO and halothane.

A

NO is not soluble in the blood.

Halothane is very soluble in blood. The more soluble agents reach equilibrium slower than less soluble agents. In other words, the blood compartment is larger for a more soluble agent.

72
Q

What determines the solubility of the gas in blood?

A

Blood/gas partition coefficient (lambda)

A gas with a higher blood gas coefficient will require higher uptake of gas into the blood and induction will be slower.

73
Q

What drives movement of the drug through the body?

A

Partial pressure

74
Q

Where does the anesthetic go first?

A

Vessel rich organs - brain, heart, liver, kidney

During maintenance, the skin and muscle start uptake. It goes to the fat latest.

75
Q

What are side effects of inhalational anesthetics?

A
  1. Decreased oxygen consumption
  2. Decreased vascular tone (decreases BP)
  3. RR becomes regular, rapid, and shallow; status asthmaticus
  4. Smooth muscle relaxation
  5. Uncoupling in the brain (increased blood flow but decreased O2 consumption)
76
Q

Which inhalational anesthetic is incomplete and has a rapid onset and recovery?

A

Nitrous oxide

77
Q

Which inhalational anesthetic has a low volatility, poor induction, and rapid recovery?

A

Desflurane

78
Q

Which inhalational anesthetic has rapid onset and recovery?

A

Sevoflurane

79
Q

Which inhalational anesthetics have a medium rate of onset and recovery?

A

Isoflurane, enflurane, halothane

80
Q

What is the main IV anesthetic and what is it used for?

A

Propofol; induction, maintenance, and sedation

81
Q

What are the effects of propofol?

A
  1. Decreased cerebral metabolic rate of oxygen (CMRO2) and ICP in the brain
  2. Veno- and arterio- dilator (preload and afterload reductions, lowers BP)
  3. Respiratory depression
82
Q

What is thiopental?

A

Barbiturate acting on GABA; most-used induction drug until propofol, not available in the US

83
Q

What are the effects of thiopental?

A

Arterial vasoconstrictor

Puts brain to sleep (vasoconstriction and decreased CMRO2)

84
Q

How does ketamine work?

A

NMDA receptor antagonist

85
Q

What are the effects of ketamine and what is it used for?

A

Dissociative anesthesia

Induction and short procedures, pain

Bronchodilator, increase CMRO2/cerebral blood flow/ICP/BP/HR

86
Q

What are the AE of ketamine?

A

Bad dreams, salivation, twitchiness

87
Q

Why is etomidate a useful drug?

A

Few cardiovascular side effects (GABA, vasoconstrictor and decreased CMRO2)

88
Q

What is the AE of etomidate?

A

Adrenal suppression

89
Q

Broadly, how do local anesthetics work?

A

Bind to sodium channels in nerves to block nerve transmission

90
Q

What are the 4 types of local anesthetics?

A
  1. Periperhal nerve blocks
  2. Neuraxial
  3. Subcutaneous
  4. Topical
91
Q

What are the indications of local anesthetics?

A
  1. Surgical anesthesia

2. Decrease post-op pain

92
Q

How does the nerve anatomy affect local anesthesia?

A
  1. Myelinated vs. non-myelinated: non- are difficult to block, most block ~3 nodes of Ranvier
  2. Core vs. mantle fibers - block works proximally first (nerve fibers innervating proximal structures are on the outside), followed by distal
  3. Smaller nerves are easier to block
93
Q

Which types of fibers are myelinated? Which are not?

A

Myelinated: A, B
Unmyelinated: C

94
Q

What are the biggest and slowest fibers? The smallest and fastest?

A

A > B > C

95
Q

What is the function of A-alpha fibers?

A

Motor

96
Q

What is the function of A-beta fibers?

A

Tactile, proprioception

97
Q

What is the function of A-gamma fibers?

A

Muscle tone

98
Q

What is the function of A-delta fibers?

A

Pain, cold temperature

99
Q

Where are B fibers located?

A

Pre-ganglionic sympathetics

100
Q

What is the function of C fibers?

A

Visceral and slow pain

101
Q

In what order are fibers blocked?

A
  1. B (small and myelinated)

2. A delta (smallest of A fibers, myelinated)

102
Q

What are the implications of a differential blockade?

A
  1. Spinal/epidural anesthesia - sympathetics go first, followed by sensory, then motor
  2. Peripheral nerve blocks - first sign may be lack of proximal muscle coordination
103
Q

What is the resting membrane potential of nerves?

A

-70 mV

104
Q

What are the three states of voltage gated sodium channels? Discuss.

A
  1. Resting: m closed, h open
  2. Activated/Open: m open, h begins to close
  3. Inactivated: h closed, m open
105
Q

Where do local anesthetics bind?

A

R site, near the h gate

106
Q

Local anesthetics preferentially bind to which states of sodium channels?

A

Activated/open and inactivated (frequency-dependent)

107
Q

What are the two groups of local anesthetics?

A

Amides (two “i” in the name) and esters (one “i” in the name)

108
Q

What are the three parts of local anesthetics?

A
  1. Benzene ring
  2. Alkyl chain (ester or amide linkage)
  3. Tertiary amine group
109
Q

List the 4 esters.

A
  1. Cocaine
  2. Procaine (Novocain)
  3. Tetracaine (Pontocaine)
  4. Benzocaine
110
Q

List the 4 amides.

A
  1. Lidocaine
  2. Mepivacaine
  3. Bupivacaine
  4. Ropivacaine
111
Q

In order to bind to the receptors, what must the anesthetic do?

A

Traverse the membrane - only the uncharged portion can cross. However, the charged form is the active form.

112
Q

If pH < pKa, what will happen?

A

Lots of H+ ions - more likely to have charged molecules

113
Q

The more lipophilic a drug is, the more ___ it will be.

A

Potent

114
Q

Proteins that bind to proteins frequently affect the duration in what way?

A

Longer duration

115
Q

What are some adjuncts to local anesthetics?

A

EPI (vasoconstriction, marker for intravascular injection)

Alpha-2 agonists (EPI, dexmedetomidine, clonidine)

116
Q

What are the indications for neuraxial anesthesia?

A

Anything from the chest down to the lower extremities

117
Q

What are the absolute contraindications for neuraxial anesthesia?

A

Patient refusal, infection at insertion site, elevated ICP, bleeding diathesis

118
Q

What are the relative contraindications for neuraxial anesthesia?

A

Bacteremia, pre-existing neurologic disease, abnormal coagulation, cardiac disease

119
Q

Where does the spinal cord terminate in adults and infants?

A

Adults: L1-2
Infants: L2-3

120
Q

Where does the dural ssac terminate?

A

S1-2

121
Q

Where are spinal taps usually done?

A

L4-5

122
Q

Discuss spinal vs. epidural blocks.

A

Spinal: subarachnoid block, needle inserted at L3-L5 (Tuffier’s line), drug deposited around cauda equina

Epidural: any level, volume-dependent segmental blockade, concentration affects quality, site of action is nerve roots

123
Q

What are the respiratory effects of neuraxial anesthesia for a blockade at the thoracic level?

A
  1. Normal tidal volume
  2. Minimal reduction in vital capacity with abdominal muscle paralysis
  3. Loss of proprioception can be upsetting to patient
124
Q

Discuss a high spinal blockade with respiratory arrest and how to treat it.

A

Never happens because of paralyzed phrenic nerves - results from hypoperfusion of the respiratory center in the 4th ventricle; treat with vasopressors and supportive ventilation

125
Q

What are the effects of neuraxial anesthesia on the vascular bed?

A
  1. Sympathectomy - arterial dilation and profound venodilation
  2. Venodilation - decreased venous return and reduced BP
126
Q

What are the affects of neuraxial anesthesia on the heart?

A

Bradycardia (due to unopposed vagal stimulation an decreased venous return - Bezold-jarisch reflex)

Cardioaccelerator fibers - T1-4

127
Q

What affects the absorption of local anesthetics?

A
  1. Vascularity (intercostal > caudal > epidural > brachial plexus > sciatic)
  2. Drug properties (protein binding, lipid solubility)
  3. Patient properties
  4. Addition of vasoconstrictors
128
Q

How are esters eliminated?

A

Plasma cholinesterase

129
Q

How are amides eliminated?

A

Liver hydrolysis by cytochrome p450

130
Q

Discuss neurotoxicity of local anesthetics.

A

Happens when inhibition of neurons > excitatory neurons
Signs/symptoms: lightheadedness, peri-oral numbness, tinnitus, seizures
Worsened by acidosis - decreased protein binding, increased cerebral blood flow

131
Q

Discuss cardiovascular toxicity of local anesthetics.

A

Occur at higher concentrations than neurotoxicity

Cardiac sodium channel bloackade, direct vasodilator effects, inhibition of SNS reflexes, neuro-mediated effects, cocaine-specific

132
Q

What are some EKG findings in cardiovascular toxicity due to LA?

A

AV conductional blockade (any degree), slurred QRS, Vfib, Vtach

133
Q

How is toxicity of LA addressed with prevention?

A

Fractionated injection with intermittent aspiration

Use of EPI as intravascular marker

Monitor patient

134
Q

How is toxicity of LA addressed with supportive therapies?

A

Maintain oxygenation and ventilation

Treat seizures

Treat arrhythmias (DO NOT USE LIDOCAINE)

135
Q

What is the antidote for LA toxicity (just cardiovascular?)?

A

Intralipid

136
Q

What allergic reactions can happen with LA?

A

Type I or Type IV hypersensitivity; almost always esters

137
Q

How can you speed the onset time for a block?

A

Add sodium bicarbonate

PT 2 (15 decks)

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