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APEX Flashcards 2025 > UNIT 5 Pharm 2 💉 > Flashcards

UNIT 5 Pharm 2 💉 Flashcards

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1
Q

What are the components of the neuron?

A

Dendrites, cell body, axon, axon terminals

Dendrites receive signals, the cell body processes them, the axon transmits signals, and axon terminals release neurotransmitters.

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2
Q

What is conduction velocity?

A

How fast an axon transmits the action potential (AP)

It is affected by myelination and axon diameter.

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3
Q

How does myelination affect conduction velocity?

A

Increases conduction velocity by allowing saltatory conduction

The AP skips along nodes of Ranvier.

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4
Q

List the three types of nerve fibers.

A

A, B, C

A fibers include alpha, beta, gamma, and delta; B fibers are preganglionic ANS; C fibers are postganglionic ANS and transmit slow pain, temperature, and touch.

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5
Q

Which nerve fiber type is blocked first by local anesthetics?

A

B fibers

These are preganglionic ANS fibers.

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6
Q

What is differential blockade?

A

The phenomenon where some fiber types are blocked sooner and easier than others

Epidural bupivacaine provides analgesia while sparing motor function at lower doses.

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7
Q

What is analogous to the ED50 for local anesthetics?

A

Minimum effective concentration (Cm)

Cm quantifies the concentration of LA required to block conduction.

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8
Q

Rank the nerve fiber types according to their sensitivity to local anesthetics.

A

B > C > small A (gamma, delta) > larger A (alpha, beta)

This ranking reflects their sensitivity to local anesthetics in vivo.

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9
Q

What are the three configurations of the voltage-gated sodium channel?

A

Resting, active, inactive

The state depends on the voltage near the channel.

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10
Q

When do local anesthetics bind to the voltage-gated sodium channel?

A

During active and inactive states

They do not bind during the resting state.

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11
Q

What is an action potential (AP)?

A

A temporary change in transmembranous potential followed by a return to transmembrane potential

It is generated when Na or Ca enters the cell, making it more positive.

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12
Q

What happens when a nerve repolarizes?

A

Removal of positive charges (K+) from inside the cell

This follows depolarization, where Na+ accumulates inside the cell.

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13
Q

How do local anesthetics affect neuronal depolarization?

A

They block Na+ channels, preventing sufficient Na+ entry for depolarization

Local anesthetics do not affect resting or threshold membrane potential.

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14
Q

What role does ionization play in local anesthetics?

A

Local anesthetics are weak bases; a higher pKa means more ionized species

The non-ionized fraction diffuses into the nerve.

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15
Q

What are the three building blocks of a local anesthetic molecule?

A

A hydrophilic group, an intermediate chain, a lipophilic group

Each affects the pharmacokinetic and pharmacodynamic profile.

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16
Q

How can you determine if a local anesthetic is an ester or an amide?

A

By the presence of two i’s in the name for amides

Amides are metabolized in the liver.

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17
Q

Contrast the metabolism of ester and amide local anesthetics.

A

Ester: metabolized by pseudocholinesterase; Amide: hepatic carboxylesterase and P450s

Cocaine is an exception, metabolized by both pathways.

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18
Q

What is the risk of allergic reactions with local anesthetics?

A

True allergy is rare; more common with esters

Allergies can be due to PABA derivatives in esters.

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19
Q

What determines the onset and action of local anesthetics?

A

pKa determines onset; closer to physiological pH = faster onset

Chloroprocaine is an exception with a high pKa but rapid onset due to higher concentration.

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20
Q

What is the primary determinant of local anesthetic potency?

A

Lipid solubility

More drug enters = more binding to Na channels.

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21
Q

What factors determine the duration of action of local anesthetics?

A

Protein binding, lipid solubility, intrinsic vasodilating activity

Protein binding is the primary determinant.

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22
Q

What is the effect of adding epinephrine to local anesthetics?

A

Extends duration of action due to vasoconstriction

This reduces the uptake of local anesthetic.

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23
Q

What is the treatment for methemoglobinemia?

A

Methylene blue 1-2 mg/kg over 5 mins

It reduces methemoglobin back to hemoglobin.

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24
Q

What are the constituents of EMLA cream?

A

50/50 of 2.5% lidocaine and 2.5% prilocaine

Prilocaine can convert to methemoglobin.

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25
What are the signs and symptoms of methemoglobinemia?
Cyanosis in the presence of normal PaO2 ## Footnote This is highly suggestive of the condition.
26
What conditions increase the risk of CNS toxicity in LAST?
Hypercarbia, hyperkalemia, metabolic acidosis ## Footnote These conditions affect the likelihood of seizures and ion trapping.
27
What modifications to ACLS treatment are needed for LAST?
Avoid epinephrine in high doses, use amiodarone, and avoid vasopressin, lidocaine, and procainamide ## Footnote Epi can hinder resuscitation and reduce lipid emulsion therapy effectiveness.
28
What is the maximum dose for EMLA cream?
5g ## Footnote This is the standard maximum recommended dose.
29
What is the treatment for LAST using lipid emulsion?
Acts as a lipid sink to sequester LA ## Footnote Bolus and infusion protocols vary by patient weight.
30
What is the most common sign of LAST?
Seizures ## Footnote Bupivacaine can lead to cardiac arrest before seizures.
31
What local anesthetics can cause methemoglobinemia?
Prilocaine and benzocaine ## Footnote They impair O2 binding and unbinding from hemoglobin.
32
What conditions allow extrajunctional receptors to populate the myocyte?
Upper/lower motor neuron injury, SCI, burns, muscle trauma, cerebrovascular accident, prolonged chemical denervation ## Footnote These conditions lead to upregulation of extrajunctional receptors.
33
What happens when succinylcholine is used in patients with upregulated extrajunctional receptors?
Transient increase in serum K by 0.5-1 mEq/L ## Footnote EJR are more sensitive to succinylcholine and remain open longer.
34
What is the risk of using Sch in a patient with upregulation of extrajunctional receptors?
Sch can transiently ↑ serum K by 0.5 -1 mEq/L for 10-15mins ## Footnote EJR are much more sensitive to Sch, leading to more K+ leakage and hyperkalemia.
35
How do extrajunctional receptors affect the clinical use of ND-NMBDs?
Upregulation results in more resistance, requiring an ↑ dose of ND-NMBD ## Footnote This is due to the increased number of receptors that are less responsive.
36
Discuss fade in the context of Sch and ND-NMBDs.
Fade occurs due to impaired mobilization of Ach, leading to only vesicles available for immediate release being used ## Footnote Sch stimulates prejunctional Nn receptors, facilitating Ach mobilization and preventing fade.
37
What is the difference between a Phase 1 and Phase 2 block?
Phase 1 has no fade; Phase 2 exhibits fade ## Footnote Sch only produces fade in a Phase 2 block.
38
What TOF ratio correlates with full recovery from neuromuscular blockade?
TOF ratio > 0.9 at the adductor pollicis
39
What is the best location to assess the onset of neuromuscular blockade?
Orbicularis oculi muscle with the facial nerve
40
How does Sch affect heart rate?
Can cause bradycardia or tachycardia ## Footnote Bradycardia is due to stimming M2-r on the SA node; tachycardia may occur by mimicking Ach at sympathetic ganglia.
41
Is Sch safe to give to a patient with renal failure?
Safe if K levels are normal to start with ## Footnote Elevated K levels can be dangerous due to the normal response to Sch.
42
How does Sch affect intraocular pressure?
Transiently ↑ by 5-15 mmHg for up to 10mins ## Footnote This is a concern in open globe airway situations.
43
List 5 names for the enzyme that metabolizes Ach.
* Acetylcholinesterase * Butyrylcholinesterase * True Cholinesterase * Plasma Cholinesterase * Erythrocyte Cholinesterase
44
What are the two classes of non-depolarizing neuromuscular blockers?
* Benzylisoquinolinium compounds * Aminosteroids
45
Discuss the metabolism of the Benzylisoquinolinium NMBDs.
Undergo spontaneous degradation in plasma; atracurium is hydrolyzed by Hofmann elimination and non-specific plasma esterases ## Footnote Cisatracurium undergoes only Hoffman elimination.
46
What factors impact Hoffman elimination?
* Blood pH * Temperature * Alkalosis and hyperthermia speed up the reaction * Acidosis and hypothermia slow down the reaction
47
What is the active metabolite of atracurium in Cisatracurium?
Laundanosine ## Footnote It is a CNS stimulant and can lead to seizures with prolonged use.
48
What drugs can potentiate the effects of NMBs?
* Volatile anesthetics * Antibiotics (aminoglycosides, clindamycin, tetracycline) * Antidysrhythmics (verapamil, amlodipine, quinidine) * Local anesthetics * Diuretics (Lasix)
49
Which neuromuscular blocker has a vagolytic effect?
Pancuronium ## Footnote It inhibits M2-r at the SA node, increasing HR and CO.
50
What is the MOA of Sugammadex?
Gamma-cyclodextrin that encapsulates NMB, making it inactive
51
What are the 3 most significant risks associated with Sugammadex?
* Anaphylaxis * CV changes (bradycardia, cardiac arrest) * Unplanned pregnancy (decreased effectiveness of hormonal contraceptives)
52
How does renal failure affect the dosing of AchE inhibitors after an aminosteroid NMBD?
Prolongs duration for both ## Footnote No need to adjust or re-dose.
53
List side effects common to AchE-I.
* Diarrhea * Urination * Miosis * Bradycardia * Bronchoconstriction * Emesis * Lacrimation * Laxation
54
Which antimuscarinics pass through the BBB?
* Atropine * Scopolamine ## Footnote They are tertiary amines, while Glycopyrrolate is a quaternary ammonium derivative.
55
In what situation can atropine cause paradoxical bradycardia?
Small doses of atropine (< 0.5 mg IV in adults) can cause this ## Footnote This occurs due to inhibition of presynaptic M1-r on vagal nerve endings.
56
How do cholinesterase inhibitors reverse paralysis caused by ND-NMB?
Reversibly inhibit AChE, allowing more ACh to exist around the NMJ
57
How do you dose Sugammadex?
58
How is Sugammadex metabolized?
Unlike roc, biliary system, sug and sug+ROC complex are excreted unchanged by the kidneys.
59
What are the 3 most significant risks associated with Sugammadex?
* anaphylaxis – 0.3% of patients * CV changes – bradycardia and cardiac arrest (anticholinergics may help this) * Unplanned pregnancy – ↓ effectiveness of hormonal contraceptives up to 7 days
60
What is the process of pain transduction?
Transduction > transmission > modulation > perception
61
What occurs during transduction?
Injured tissue releases various chemicals that activate peripheral nerves and/or cause immune cells to release pro-inflammatory compounds.
62
What type of nerve fibers transmit pain?
* A-delta: fast, sharp, localized pain * C-fibers: slow, dull, diffuse
63
What is the role of inflammation in pain transduction?
Inflammation contributes to: * ↓ threshold to pain stimulus (allodynia) * ↑ response to pain stimulus (hyperalgesia)
64
What is the process of pain transmission?
Pain signal is relayed through the 3-neuron afferent pathway along the spinothalamic tract.
65
What are the 3 neurons involved in pain transmission?
* 1st order neuron: periphery 🡪 dorsal horn (cell body in dorsal root ganglion) * 2nd order: dorsal horn 🡪 thalamus (cell body in dorsal horn) * 3rd order: thalamus 🡪 cerebral cortex (cell body in thalamus)
66
What is the process of pain modulation?
The pain signal can be modified (inhibited or augmented) as it advances towards the cerebral cortex.
67
Where does the DIC pathway begin?
The DIC pathway begins in the periaqueductal gray and rostroventral medulla.
68
What neurotransmitters are involved in the inhibition of pain?
* GABA * Glycine * NE * 5HT * Endorphins
69
What causes pain augmentation?
* Central sensitization * Wind-up
70
What occurs during pain perception?
Processing of afferent pain signals in the cerebral cortex and limbic system.
71
What is the MOA of opioids?
Opioid-r links to GPCR and agonism of the receptor instructs the G protein to ‘turn off’ AC 🡪 ↓ intracellular cAMP (2nd msgr) 🡪 alters ionic currents and ↓ neuronal function.
72
What are the precursors of endogenous opioids?
* Pre-proopiomelanocortin 🡪 endorphins (Mu-r) * Pre-enkephalin 🡪 enkephalins (delta-r) * Pre-dynorphin 🡪 Dynorphins (kappa-r)
73
What are the physiologic effects of mu-1, mu-2, mu-3 receptor stimulation?
* Are most important
74
What are the unique effects of kappa stimulation?
* Anti-shivering * Diuresis * Dysphoria * Delirium * Hallucinations
75
How do opioids affect HR, BP, and myocardial function?
* HR: ↓ from mu2 stim; meperidine can ↑ HR * BP: minimal effects, if healthy; HoTN likely from histamine release * Myocardial function: contractility NOT affected; depression can occur if combined with N2O
76
How do opioids affect ventilation?
Stim mu and delta-r (possibly kappa): ↓ ventilatory response to CO2, ↓ RR and compensatory ↑ Vt, ↑ PaCO2 🡪 ↑ ICP if ventilation is not maintained.
77
How do opioids affect the pupil?
Edinger Westphal nucleus stimulation 🡪 ↑ PNS stim of ciliary ganglion and oculomotor nerve (CN3) 🡪 pupil constriction.
78
How do opioids produce nausea/vomiting?
Mu-r stimulation of the chemoreceptor trigger zone (area postrema of medulla).
79
How do opioids affect biliary pressure, gastric emptying, and peristalsis?
* Biliary pressure: contraction of sphincter of Oddi = ↑ pressure * Gastric emptying: prolonged * Peristalsis: slowed = constipation
80
How do opioids contribute to urinary retention?
* Detrusor relaxation * Urinary sphincter contraction
81
What are the immunologic effects of opioids?
* Histamine release * Inhibition of cellular & humoral immune function * Suppression of natural killer cell function
82
How do opioids affect thermoregulation?
They reset the hypothalamic temp set point = ↓ core body temp.
83
Rank IV opioids in terms of potency.
MMHARFS (least 🡪 most): * meperidine < morphine < hydromorphone < alfenta < remifent = fent < Sufenta
84
What opioids produce an active metabolite?
* Morphine * Meperidine
85
What is the active metabolite of morphine and why is it a problem?
Morphine-3-glucuronide (inactive) and morphine-6-glucuronide (active); impaired renal function = ↓ MP6 excretion = accumulation = resp depression.
86
What is the active metabolite of meperidine and why is it a problem?
Normeperidine is ½ potent; ↓ SZ threshold and ↑ CNS excitability.
87
Discuss the co-administration of meperidine and MAOi.
Can cause serotonin syndrome; meperidine is a weak serotonin reuptake inhibitor.
88
How does the ionization characteristics of alfentanil influence its onset of action?
Fastest onset; pKa = 6.5 (less than physiologic pH); 90% non-ionized.
89
Which opioid has the largest Vd? Smallest?
* Largest = fentanyl (4L/kg) * Smallest = remifent (0.39L/kg)
90
Discuss PK/PD profile of remifentanil.
Rapid on and rapid-off mu agonist; 4 min CSHT; has an ester linkage.
91
Discuss the relationship between remifentanil and opioid-induced hyperalgesia.
Causes acute opioid-induced hyperalgesia following DC; ketamine or MgSO4 can prevent OIH.
92
Can remifentanil be used for neuraxial anesthesia? Why or why not?
No; remi powder mixed with a free base and glycine can cause skeletal muscle weakness.
93
How does methadone reduce pain?
* Mu-r agonist * NMDA-r antagonist * Inhibits reuptake of monoamines
94
Which opioid is most likely to cause QT prolongation?
Methadone can cause Torsades de pointes.
95
What is the etiology of opioid-induced skeletal muscle rigidity?
Rapid IV admin of potent IV opioids can cause this (mu-r stim in the CNS).
96
What is the treatment of opioid-induced skeletal muscle rigidity?
Paralysis + intubation; naloxone may not be effective if given just before surgery.
97
What are the common characteristics of opioid partial agonists?
* Agonists-antagonists can never achieve the same intensity as a full agonist * Produce analgesia with a reduced risk of respiratory depression * Have a ceiling effect
98
Compare/contrast buprenorphine, nalbuphine, butorphanol.
99
Discuss the potential complications of opioid reversal with Naloxone.
* Short duration (30-45 mins) * SNS stimulation * N/V
100
Which opioid antagonist is least likely to reverse respiratory depression? Why?
Methylnaltrexone; it cannot pass the BBB.
101
Which opioid antagonist has the longest duration of action?
Naltrexone; PO has duration of 24hrs.

APEX Flashcards 2025 (6 decks)

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