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Review > Chapter 19 Pharmacology for the Interventional Pain Physician > Flashcards

Chapter 19 Pharmacology for the Interventional Pain Physician Flashcards

1
Q

Iodinated contrast agents provide greater attenuation

of x-ray radiation, relative to

A

tissue and bone, reducing
the amount of radiation reaching the detector (fluoroscopic intensifier) This allows contrast to be easily visualized on x-ray images

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2
Q

Iodinated contrast media (ICM)

in image-guided procedures is utilized to

A

define the anticipated spread and location of the injectate. This improves safety by avoiding injection of drugs into unintended locations such as intravascular or intrathecal
spaces

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3
Q

ICM are based on variations of

A

the 2, 4, 6 tri-iodinated benzene ring

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4
Q

ICM are classified on the basis of

A

their chemical structure, osmolality, iodine content, and ionization

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5
Q

The iodine content is responsible for

A

x-ray attenuation and the concentration in mg iodine/ml is used to express the strength of the
attenuation of a particular agent

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6
Q

Clinically used ICM agents

have how much iodine

A

between 180 to 400 mg/ml of iodine.

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7
Q

The chemical composition of contrast media is in four different forms:

A

ionic monomers,
ionic dimers,
nonionic monomers
nonionic dimers

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8
Q

Ionization of ICM is produced

by

A

substitutions on the benzene ring at the 1, 3, and 5 positions to produce water solubility and physiologic pH

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9
Q

Solubility of the nonionic contrast media is due to

A

substitution with hydrophilic side chains such as

hydroxyl or amide groups

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10
Q

The concentration of iodine necessary to obtain

radiographic attenuation dictates

A

the number of particles in solution (osmolality) needed for a particular agent to be effective

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11
Q

Contrast osmotoxic reactions

A

pain on injection, hemolysis,
endothelial damage (capillary leak and edema), vasodilation
(flushing, warmth, hypotension, and cardiovascular
collapse), hypervolemia, and direct cardiodepressive effects

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12
Q

Ionic ICM are strictly contraindicated for all applications involving the

A

central nervous system (CNS) and may cause severe or fatal neurotoxic reactions following
intrathecal administration

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13
Q

ICM agents of choice for interventional pain procedures

A

Non-ionic ICM are the agents of choice due to their lower osmolality and toxicity

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14
Q

Commercially Available Ionic Monomeric X-ray Contrast Media

A 
Meglumine iothalamate (Conray)
Meglumine ioxithalamate (Telebrix)
Sodium amidotrizoate (Urografin, Hypaque)
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15
Q

Commercially Available Nonionic Monomers X-ray Contrast Media

A 
Iohexol (Omnipaque)
Iopentol( Imagopaque)
Ioxitol ( Ixilan)
Iomeprol (Iomeron)
Ioversol (Optiray)
Iopromide (Ultravist)
Iobitridol (Xenetix)
Iopamidol (Iopamiro)
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16
Q

Commercially Available Ionic Dimer X-ray Contrast Media

A

Ioxaglate (Hexabrix)

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17
Q

Commercially Available Non- Ionic Dimer X-ray Contrast Media

A

Iotrolan (Isovist)

Iodixanol (Visipaque)

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18
Q

ICM Distribution

A

ICM are hydrophilic and demonstrate low protein binding. After intravascular injection there is rapid
distribution into the extracellular space and the fall in plasma concentration is rapid.

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19
Q

ICM Metabolism

A

Elimination is by glomerular filtration without reabsorption and there is virtually no metabolism.

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20
Q

ICM Elimination in patient with and without renal impairment.

A

In patients with normal renal function the elimination half-life is approximately 2 hr, and with renal impairment excretion can last for weeks.

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21
Q

Severe reactions of ICM

A

anaphylactic or anaphylactoid symptoms of severe bronchospasm, laryngeal edema, angioedema, pulmonary edema, hypotension, convulsions, cardiac dysrhythmias, or arrest

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22
Q

Adverse reactions to ICM can be classified as

A

idiosyncratic or immediate and delayed.

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23
Q

The immediate reactions of ICM

A

are generally the most severe and consist in this setting of
anaphylactoid type reactions of varying severity. These reactions are generally independent of dose and unpredictable, and usually occur within 1 hr of administration. There is increased risk in patients with a prior reaction to ICM, and with underlying disease including asthmatics,history of atopy, and advanced heart disease

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24
Q

Treatment of immediate reactions of ICM

A

If suspected these reactions need to be treated with antihistamines,
epinephrine, corticosteroids, and full cardiopulmonary
resuscitation as needed

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25
Q

Delayed reactions of ICM

A

Delayed reactions are composed of chemotoxic reactions and cutaneous manifestations of delayed hypersensitivity. The chemotoxic reactions
include contrast mediated nephrotoxicity, decreased cardiac
contractility, and neurotoxicity, all of which are dose
dependent and should be rare in this setting with use of
nonionized agents.

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26
Q

The delayed allergy-like skin reactions of ICM

A

are twice as frequent for nonionic dimers as for nonionic monomers

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27
Q

How to prevent adverse reactions of ICM?

A

The first step is to understand the risk factors, including a previous reaction to ICM, and take a history to elucidate the type of reaction the patient experienced. The history should also include the type of agent and whether it was an ionic or nonionic agent

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28
Q

Treatment protocols for anaphylactic and anaphylactoid reactions,

A

antihistamine and corticosteroid prophylaxis against anaphylactic and anaphylactoid reactions,
including oxygen, intravenous fluids, antihistamines (H1 and H2blockers), adrenergic drugs (epinephrine), and corticosteroid

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29
Q

Ionic ICM vs. non-ioninc agents adverse reactions

A

Ionic ICM have 4 times the incidence of these reactions

compared to nonionic agents

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30
Q

Gadolinium containing

contrast agents

A

the use of gadolinium containing contrast agents beneficial as an alternative in
high-risk patients. However, there is an upper limit to safe
dosage of gadolinium (0.3 mmol/kg body weight)

31
Q

Adverse Effects of Gadolinium containing contrast agents

A

caution and reduced dosage have to be taken in patients

with moderate to severe renal dysfunction due to its association with development of nephrogenic systemic fibrosis

32
Q

Local anesthetics Mechanism of Action

A

LAs prevent generation and conduction of the nerve impulse by blocking voltage gated Na+ channels within
the cell membrane. This reduces or prevents the transient increase in Na1+ permeability needed for depolarization and propagation of a nerve impulse.

33
Q

Akyl substitutions on a LA increase

A

the lipid solubility

34
Q

The potency of LAs have been shown to be directly related

to

A

lipophilicity and is often expressed as the octanol:water partition coefficient

35
Q

Local anesthetics Acid or Base?

A

All LAs are weak acids as quaternary amines and are positively charged. As tertiary amines they are weak bases
and uncharged

36
Q

Local anesthetics be in what form to access their site of action on the Na+ channel?

A

They must be in their lipophilic base form

to access their site of action on the Na+ channel

37
Q

pKa of the Local anesthetics

A

The pKa of the LA and pH at the site of injection (usually physiologic pH of 7.4 but can be locally altered, such as in areas
of infection) influence the amount of LA in base form and the speed of block onset. In general, the lower the pKa of the LA the faster its the onset.

38
Q

The addition of bicarbonate to a

solution does what to local anesthetics?

A

The addition of bicarbonate to a
solution to increase the pH and speed of onset can be done to epinephrine-containing LAs that are adjusted to an acidic pH for stability

39
Q

factors influencing the speed of onset include

A

the concentration and amount of LA used and the anatomic location of injection or application

40
Q

Fibers response to local anesthetics

A

small unmyelinated C-fibers, autonomic fibers,
and small myelinated Ad delta fibers (pain and temperature)
are more sensitive than larger myelinated
Ag, Ab, and Aa fibers (motor, proprioception, touch, and
pressure.

41
Q

Ropivacaine vs. Bupivacaine

A

More recently, ropivacaine, is stated

to be more motor sparing than bupivacaine and less cardiotoxicity at equipotent doses

42
Q

multiple factors

that determine duration of action

A

Increased lipid solubility
increases its duration of action. the rate of metabolism can be a factor (e.g., amino-ester LAs). the speed of
uptake and/or elimination from the site of deposition, which is also dependent on tissue perfusion, influences the
duration of action. addition of vasoconstrictors to
decrease perfusion and uptake and thus prolong block

43
Q

Perfusion of course is dependent on anatomic location

A

parauterine > intercostal >epidural > peripheral nerve >intrathecal

44
Q

TABLE 19–2

A

Infiltration Anesthesia

45
Q

most common adverse reactions of local anesthetic

A

The most common adverse reactions are autonomic responses or anticipatory reactions to medical procedures.
These include tachycardia, sweating, hypotension, and
syncope. They are characteristically short-lived with resolution
in minutes requiring no treatment or can be treated with muscarinic blockers or ephedrine

46
Q

common reaction is the response to vasoconstrictor

additives, usually epinephrine

A

Symptomatically
this produces tachycardia, hypertension, and anxiety or feelings
of doom. If injected peri- or intra-arterial it can produce distal ischemia from arterial spasm

47
Q

systemic toxicity of local anesthetics results first in the CNS and then has cardiovascular effects

A

CNS symptoms
consist of metallic taste, perioral numbness, dizziness, muscle twitching, and ultimately generalized seizures.
Toxic cardiovascular effects include arrhythmias, cardiac
depression, vasodilation, hypotension, and cardiac arrest/
collapse

48
Q

Trearment of bupivacaine-induced cardiac toxicity

A

The use of 20% intralipid has been shown to be effective for resuscitation from bupivacaine-induced cardiac toxicity

49
Q

Allergic reactions to LAs due to

A

The vast majority

of these are due to PABA from amino-ester LAs. Amino-amide LAs are exceedingly rare causes of allergic reactions

50
Q

Paraben preservatives

A

Paraben preservatives are structurally very
similar to PABA and can show allergic cross-reactivity to
amino-ester LAs

51
Q

The commonest allergic reactions of LA are

A

delayed (24 hrs to a week) minor cutaneous rashes. These
are generally self-limited and treated with antihistamines
and topical corticosteroids

52
Q

allergic cross-reactivity to bisulfite preservatives in patients with

A

known food allergies and paraben preservatives in

patients with sulfa antibiotic allergY

53
Q

A high level or complete

spinal block will result in

A

respiratory compromise by diaphragmatic and accessory muscle paralysis and in total
sympathectomy

54
Q

Treatment of High Spinal

A

Immediate resuscitation can be required,

including respiratory and cardiovascular support

55
Q

Adverse Effects of Local Anesthetics

A

Intrathecal
administration of some LAs (lidocaine, chloroprocaine)
and additives (metabisulfite) are suspected of causing toxic effects ranging from transient neurologic symptoms (TNS)
to adhesive arachnoiditis and permanent neurologic injury.

56
Q

Naturally occurring corticosteroids are classified into three
functional groups

A

mineralocorticoids, glucocorticoids,

and adrenal androgens.

57
Q

corticosteroid

most commonly used for interventional pain procedures.

A

Glucocorticoids

58
Q

mechanisms of action for corticosteroids

A

antiinflammatory effects, direct neural membrane stabilization, as well as modulation of peripheral nociceptor neurons and spinal cord dorsal horn cells

59
Q

The anti-inflammatory effects of glucocorticoids are attributable to

A

their inhibition of inflammatory mediator production at both the local tissue and systemic immune response level

60
Q

With any type of tissue trauma there is a release of inflammatory mediators including

A

arachidonic acid and its

metabolites (prostaglandins, leukotrienes), various cytokines (IL-1, IL-6, TNF-a), and other acute phase reactants

61
Q

mechanisms of action for injected corticosteroids

A

inhibit the production of local inflammatory mediators, reduced spontaneous ectopic discharge rates seen following nerve injury, including in neuromas.. Reversible inhibition
of nociceptive C-fiber transmission, but not A-B fiber transmission

62
Q

glucocorticoid receptor sites within the dorsal horn

A

glucocorticoid receptor sites have been located on noradrenergic and 5-hydroxytryptamine neurons within the dorsal horn substantia gelatinosa—known pathways of pain transmission. This suggests that corticosteroids may modulate nociceptive input from peripheral
nociceptors by a direct action on the spinal cord.

63
Q

the anti-inflammatory efficacy and duration of activity are greater with

A

less soluble corticosteroid

preparations

64
Q

major determinant
of corticosteroid selection
based upon

A

its duration of action (biological half-life) and antiinflammatory
potency, but steroid particulate size relative to a red blood cell and aggregation is emerging as a major determinant
of corticosteroid selection

65
Q

An inadvertent injection of a steroid particulate into the artery of Adamkiewicz during thoracic or lumbar transforaminal epiduralsteroid injection could result in

A

spinal cord ischemia leading to profound lower extremity motor deficits, even paraplegia

66
Q

complication of cervical level transforaminal

steroid injection

A

is infarction of the spinal cord or brain
following injection of a particulate corticosteroid into a
radicular artery or vertebral artery

67
Q

Following systemic absorption, the vast majority of
corticosteroid is reversibly bound to two plasma proteins:
.

A

corticosteroid-binding globulin and albumin

68
Q

the unbound and bound fraction of corticosteroid

A

the unbound fraction of corticosteroid is responsible for its cellular-mediated anti-inflammatory effects. The protein-bound corticosteroid undergoes sequential oxidative-reduction reactions yielding inactive compounds. This is followed by hepatic-mediated
conjugation (sulfate or glucuronide), resulting in watersoluble
metabolites that are renally excreted

69
Q

adverse reactions following corticosteroid injection.

A

Sterile meningitis
and arachnoiditis have been reported following intrathecal injection of methylprednisolone.Brief euphoric or manic reactions have been reported following high-dose conticosteroid
therapy. analphylactoid reactions have been reported following intravenous, intramuscular,
and soft-tissue conrticosteroid injections

70
Q

Any type of anaphylactic reaction should be treated promptly and aggressively with

A 
supportive therapies (i.e., airway, breathing, circulation, supplemental oxygen),
including advanced cardiac life support guidelines when indicated
71
Q

Potential Adverse Systemic Reactions Associated

with Corticosteroids

A

Fluid retention, Elevated blood pressure, Hyperglycemia, Generalized erythema/facial flushing
Menstrual irregularities, Gastritis/peptic ulcer disease, Hypothalamic-pituitary-adrenal axis suppression, Cushing’s syndrome
Bone demineralization
Steroid myopathy
Allergic reaction

72
Q

aqueous-based or alcohol-based skin preparation solutions.

A

Aqueous-based
iodophors, such as povidone-iodine, can be safely used on
mucous membrane surfaces. Alcohol-based solutions offer a
quicker onset and often more sustained antimicrobial activity.

73
Q

The ideal preoperative skin antiseptic agent should

A

significantly reduce microbial counts on intact skin; be broad spectrum; be fast acting; have a persistent effect lasting for hours; and
be nonirritating to the skin

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