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Pharmacology 1 choefsho > Analgesics (local anesthetics, NSAIDS, opioids, others) > Flashcards

Analgesics (local anesthetics, NSAIDS, opioids, others) Flashcards

1
Q

______________________ cause reversible blockade of transmission in peripheral nerves or spinal cord, usually to stop pain signals

A

Local anesthetics cause reversible blockade of transmission in peripheral nerves or spinal cord, usually to stop pain signals

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2
Q

Chemically, local anesthetics consist of an aromatic group joined to a tertiary amine group by either an _________ or _________ group.

A

Chemically, local anesthetics consist of an aromatic group joined to a tertiary amine group by either an amide or ester group.

  • Aromatic ring improves lipid solubility
  • Terminal amine may be in tertiary (nonionized) or quaternary (ionized) form
  • Amide vs. ester group affect metabolism
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3
Q

Where are esters metabolized?

A

Hydrolyzed by plasma esterases (blood)

  • Ester local anesthetics: procaine, proparacaine, benzocaine, tetracaine, cocaine
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4
Q

Where are amides metabolized?

A

Liver

  • Amide local anesthetics: lidocaine, bupivacaine, mepivacaine, ropivacaine, prilocaine, dibucaine
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5
Q

What is the mechanism of action for local anesthetics? How do they work?

A

They block voltage-gated sodium channels in nerve axons

  • Sodium channels exist in the resting state, open state (action potention), and inactivated state (refractory period)
  • Most local anesthetics (pKA 8-9) cross the neuron cell membrane in the unionized form and need to be ionized to interact with a receptor inside of the cell
  • LAs have a higher affinity for the open and inactivated states
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6
Q

T or F. Vasoconstriction decreases the distribution of local anesthetics away from the site of action.

A

True (can be enhanced with local epinephrine)

  • The clinical action is terminated by redistribution (no action when the drug leaves the area)
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7
Q

How are local anesthetics eliminated from the body?

A
  • Ester LAs are rapidly broken down by plasma pseudocholinesterases
  • Amide LAs are mainly metabolized in the liver
  • Metabolites are excreted in the urine
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8
Q

What are the routes of administration for local anesthetics?

A
  • Topical
    • Skin (what formulations?) or splash block
  • Injection/local infiltration (ex. ring block)
    • Peripheral nerve block, intra-articular (joint block in equine for lameness exams), epidural/intrathecal
  • Intravenous regional anesthesia
    • Brier’s block

Directly to the site of action

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9
Q

Which type of nerve fibers do local anesthetics work most easily on? (put it in order)

  1. Myelinated sensory (A alpha/beta fibers)
  2. Myelinated motor (A alpha fibers)
  3. Unmyelinated sensory (C fibers)
  4. Thinly myelinated (A delta fibers)
A
  1. Unmyelinated sensory > 4. Thinly myelinated > 1. Myelinated sensory > 2. Myelinated motor
  • Unmyelinated sensory: warm perception, chronic pain
  • Thinly myelinated: cold perception, acute pain
  • Myelinated sensory: touch, vibration, position, perception
  • Myelinated motor: muscle control
  • Need more LA to affect muscle control
  • Pain and sympathetic transmission is blocked before motor transmission
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10
Q

What are frequency-dependent blocks?

A

Rapidly firing nerves will be preferentially blocked

  • Nerve fibers carrying pain signals
  • Antiarrhythmic
  • Anticonvulsant
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11
Q

The dose of local anesthetics can be increased by increasing the ____________ or the ___________ at the target site.

A

The dose of local anesthetics can be increased by increasing the volume or the concentration at the target site.

  • The larger the dose, the more rapid the onset of action and sometimes longer duraction of action
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12
Q

Potency increases by increasing __________ and __________ solubility of the drug.

A

Potency increases by increasing lipid and water solubility of the drug.

  • Lipophilicity increases penetration into the cell and therefore binding with sodium channels
  • Hydrophilicity increases diffusion to the site of action
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13
Q

The onset of action of local anesthetics depend on what 3 factors?

A
  1. Placement of the drug concentration
  2. Concentration used
  3. Drug factors (molecule size, lipophilicity, protein binding, pKa); the lower the pKa the more unionized drug to penetrate into the axonal cell
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14
Q

The duration of action depends on what 3 factors?

A
  1. Lipophilicity (drug penetration into the axon)
  2. Binding to the sodium channel
  3. Continuous presence or absence at the site of action (vasoconstrictors)
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15
Q

Which of the following is not a clinical use of local anesthetics?

  1. Operative analgesia
  2. Pre and post-operative analgesia for surgery
  3. Treatment of ventricular arrhythmias
  4. Regional anesthesia
  5. All of the above are clinical uses
A
  1. All of the above are clinical uses
  • Operative analgesia (usually with sedation)
    • e.g. LDA (left displaced abomasum) surgery in ruminants
  • Pre and post-operative analgesia for surgery
    • Nerve blocks, line blocks, and epidurals
  • Treatment of ventricular arrhythmias
    • Systemic use- NOT WITH EPINEPHRINE!
  • Regional anesthesia
    • For minor procedures (e.g. skin biopsy) and lameness localization (e.g. nerve blocks in equine)
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16
Q

Which of the following is not an adverse effect of local anesthetics?

  1. Muscle twitching and tremors
  2. Convulsive seizures
  3. Unconsciousness
  4. Respiratory arrest
  5. Bradycardia and dysrrhythmias
  6. Decreased contractility
  7. Vasoconstriction
A
  1. Vasoconstriction; it can cause VASODILATION and HYPOTENSION

Adverse effcts:

  • CNS stimulation: muscle twitching, tremors, convulsive seizures
    • Treat with diazepam or midazolam
  • CNS depression: unconsciousness, respiratory arrest
    • Treat with artificial respiration
  • Cardiovascular depression: bradycardia, dysrrythmias, decreased contractility, vasodilation, hypotenision; the more potent the LA, the greater the myocardial depression
  • Local irritation of skeletal muscles and nerves at the injection site
  • Methemoglobinemia due to toxic metabolites with some LAs (Benzocaine, prilocaine)
  • Histamine release seen with ester LAs (and lidocaide preservative methlparaben) due to metabolite PABA
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17
Q

Which ester local anesthetic is not used as a local anesthetic, but is in some Penicillin G preparations?

  1. Bupivacaine
  2. Lidocaine
  3. Procaine
  4. Proparacaine
  5. Mepivacaine
A
  1. Procaine
  • It slows the absorption at IM injection sites (Pen G), NEVER GIVEN IV
  • Slow onset and short duration of action
  • Poor penetration of mucous membranes
  • Metabolized to PABA
  • Toxic (esp. in horses); CNS stimulation (excitement, seizures)
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18
Q

What is the most commonly used amide local anesthetic in veterinary medicine that is used as a local anesthetic and systemically?

  1. Bupivacaine
  2. Lidocaine
  3. Procaine
  4. Proparacaine
  5. Mepivacaine
A
  1. Lidocaine (Xylocaine)
  • Banned in Europe for food producing animals (due to metabolite 2,6-xylidine that may be a carcinogen)
  • Rapid onset (5 minutes), medium duration (40-60 minutes; longer if given with epinephrine)
  • Sheep are most sensitive species
  • Cats are more sensitive than dogs
  • May contain epinephrine 1:200,000
  • Used as 1-2% solution parenterally or 4% solution topically (gels, ointments, sprays, patches, EMLA cream)
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19
Q

What is lidocaine used for systemically?

A

REMEMBER, NO EPINEPHRINE with SYSTEMIC LIDOCAINE!

  • Class 1B antiarrhythmic used to control ventricular arrhythmias (ventricular tachycardia)
  • CRI as an adjunctive analgesic
    • “MLK” drips (morphine-lidocaine-ketamine)
    • Lidocaine patches are available
  • CRI as a GI prokinetic/anti-inflammatory
    • Used to treat/prevent post-op ileus in horses, humans
    • Prevention of reperfusion injury/endotoxemia?
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20
Q

Why is lidocaine (local use/analgesia) mixed with sodium bicarbonate (9:1) before local injection?

A

To reduce pain on injection

  • It may alter clinical effect
  • Possible risk of precipitation
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21
Q

Which specific local anesthetic is used mainly in humans to facilitate percutaneous catheterization? Why would it be preferred over lidocaine?

A

5% EMLA cream (contains 2.5% lidocaine/ 2.5% prilocaine); preferred over lidocaine because it has lower toxicity

  • 20-30 minutes to full effect
  • Dermal analgesia (5mm depth)
  • Prilocaine is also used for intravenous regional anesthesia
  • Methemoglobinemia possible due to metabolic by-products
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22
Q

Which amide local anesthetic is frequently used for nerve blocks and epidurals, but has a slow onset and is the most cardiotoxic of the local anesthetics?

  1. Bupivacaine
  2. Lidocaine
  3. Procaine
  4. Proparacaine
  5. Mepivacaine
A
  1. Bupivacaine (Marcaine)
  • Used for local infiltration, nerve blocks, epidurals
  • 0.5% solution for injection
  • Slow onset (20 mins) but long duration (up to 8 hours)
  • MOST cardiotoxic, more potent than lidocaine; diazepam may increase cardiodepressant effects
  • NOT used topically
  • Ropivacaine is a racemic mixture (S enantiomer) that is less cardiotoxic
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23
Q

Which amide local anesthetic is used for diagnostic nerve blocks in horses and is preferred over lidocaine because it is less irritating?

  1. Bupivacaine
  2. Lidocaine
  3. Procaine
  4. Proparacaine
  5. Mepivacaine
A
  1. Mepivacaine (Carbocaine)
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24
Q

Which local anesthetic is used topically as an opthalmic formulation to allow for corneal and conjunctival manipulation (e.g. testing intraocular pressure with a tonopen)?

  1. Bupivacaine
  2. Lidocaine
  3. Procaine
  4. Proparacaine
  5. Mepivacaine
A
  1. Proparacaine (Alcaine)
  • Rapid onset (30 seconds!), short duration (10-20 minutes)
  • Less irritating than other ophthalmic options (e.g. tetracaine)
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25
Q

Nonsteroidal anti-inflammatory drugs (NSAIDs) prevent inflammation by inhibiting ________________ enzymes.

A

Cyclooxygenase (COX) enzymes

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26
Q

T or F. NSAIDs are weak acids.

A

True

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27
Q

What do glucocorticoids target?

A

Phospholipases

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28
Q

Constitutive, physiologic production of prostaglandins that play an important role in normal homeostasis.

  1. COX-1
  2. COX-2
A
  1. COX-1
  • TXA2 promotes platelet aggregation
  • PGE1 is involved with GI mucosal maintenance and vasodilation in the kidney in response to decreased blood flow
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29
Q

Inducible, prostaglandins produced during inflammation.

  1. COX-1
  2. COX-2
A
  1. COX-2
  • These are not absolute distinctions (between COX-1 and COX-2) as once thought, but for routine analgesia/anti-inflammatory uses greater COX-2 selectivity is generally preferable
  • WE WANT TO TARGET COX-2 SPECIFICALLY!
30
Q

Matching!

A. COX-1 selective inhibitors

B. Nonspecific COX inhibitors

C. COX-2 preferential inhibitors

D. COX-2 selective inhibitors

  1. Firocoxib, robenacoxib
  2. Acetylsalicylic acid (ASA)
  3. Deracoxib, carprofen, meloxicam
  4. Flunixin, ketoprofen, phenylbutazone
A

A. COX-1 selective inhibitors: 2. Acetylsalicylic acid (ASA)

B. Nonspecific COX inhibitors: 4. Flunixin, ketoprofen, phenylbutazone

C. COX-2 preferential inhibitors: 3. Deracoxib, carprofen, meloxicam

D. COX-2 selective inhibitors: 1. Firocoxib, robenacoxib

31
Q

T or F. Prednisone/prednisolone (glucocorticoids) can be used with NSAIDs to give a synergistic effect.

A

FALSE! DO NOT USE NSAIDS AND STEROIDS TOGETHER!

32
Q

What are the routes of administration for NSAIDs?

A

PO or IM

  • May adsorb to feed (reduce absorption)- phenylbutazone and flunixin > less bioavailability
33
Q

T or F. NSAIDs are highly protein bound which results in a low volume of distribution.

A

True

  • 95-99% protein bound
  • In the face of inflammation there may be extravasation of plasma proteins (carrying drug with it)
  • Displacement may occur if used concurrently with other highly protein bound drugs (Warfarin)
  • Can penetrate into the CNS but do not distribute into milk
34
Q

Where are NSAIDs metabolized and eliminated?

A

Hepatic metabolism (phase I and phase II) and elimination via urine (with some unchanged drug being eliminated)

  • Metabolism differs between species, between breeds, and inter-individual differences
    • E.g. dogs who expressed CYP215 (45%) enzyme metabolize celecoxib 3x faster than dogs who do not (some dogs will get toxic effects with same dose)
    • Some NSAIDs are converted to active metabolites
      • Acetylsalicylic acid > salicylic acid
      • Phenylbutazone > oxyphenbutazone
  • Biliary excretion and enterohepatic recirculation can be seen with some NSAIDs
35
Q

T or F. Since you know that you can give your 20 pound dog X mg/kg, you can extrapolate the dose to your 2000 pound cow to 100X mg/kg.

A

False! DO NOT extrapolate dose rates or intervals from one species to another; terminal half-life varies considerably between species

36
Q

Anti-inflammatory effects of NSAIDs work by inhibiting the synthesis of _____________.

A

Eiconsanoids (thrombaxane, prostacyclin, prostaglandins)

  • NSAIDs are not as potent anti-inflammatory agents as glucocorticoids (steroids)
    • But they do not delay wound helaing or cause immunosuppression
    • Greater effect on acute inflammation than chronic (which is more for pain)
37
Q

T or F. NSAIDs provide analgesia only if there is inflammation present.

A

False, it provides analgesia whether inflammation is present or not

  • Decreases sensitization of neurons
    • To bradykinin peripherally
    • Centrally (interaction of prostaglandins with nociception)
38
Q

T or F. Antipyretic effects (fever reducing) of NSAIDs will reduce hyperthermia and also lower normal body temperature.

A

False! It will not reduce hyperthermia or normal body temperatures

  • It targets fever caused by endotoxins
    • Endotoxins produce IL-1 > hypothalamus > PGE2 > increase thermoregulatory ‘set point’ > fever
  • The underlying cause for fever should be diagnosed and addressed!
39
Q

T or F. Antiendotoxic effects of NSAIDs are beneficial if given before endotoxic challenge.

A

True

  • Unclear how much benefit there is if given after
40
Q

Antithrombotic effects of NSAIDS, such as low dose acetylsalicylic acid (Aspirin), are due to the inhibition of _____________.

A

Thromboxane A2 (TXA2)

  • Preferential, irreversible inhibition of COX in platelets
    • TXA2 is a platelet aggregating agent (inhibited)
    • PGI2 is an anti-aggregating agent (less inhibited)
  • Increased clotting time (doesn’t resolve clots, but helps reduce further clots)
41
Q

How are NSAIDs capable of having antineoplastic effects?

A

COX-2 is expressed by a number of cancers and use of NSAIDs is associated with improved outcomes

  • Transitional cell carcinoma (TCC) and osteosarcoma
  • Piroxicam (Feldene) is often used for this purpose
42
Q

In what 3 acute conditions would NSAIDS be used clinically?

A
  1. Inflammation
    • Dampen inflammatory response in infectious disease
    • Treat acute inflammatory conditions
    • Postoperative
  2. Antipyretic (reduce fever)
  3. Endotoxemic syndromes (?)
43
Q

In what 3 chronic conditions would NSAIDs be used clinically?

A

Chronic conditions = NSAIDs used primarily for pain

  1. Chronic osteoarthritis: MOST COMMON USAGE IN SMALL ANIMALS
  2. Antithrombotic (reduce platelet aggregation)
  3. Adjunct therapy for neoplasia
44
Q

What are the 3 body systems that NSAIDs have adverse effects on?

A

GI, kidneys, and liver

45
Q

Why would NSAIDs cause gastrointestinal irritation and ulcerations?

A

Prostaglandins are involved in the maintenance of normal GI homeostasis (keep high mucosal blood flow, promote turnover of mucosal cells, production of mucus/bicarbonate, etc.)

  • If we inhibit prostaglands with NSAIDs, this can result in GI ulcers, right dorsal colitis, abomasal ulcers, and other GI irritations
  • Risk of ulcers is significantly increased by concurrent use of steroids SO NEVER USE NSAIDS AND STEROIDS TOGETHER
46
Q

Why would the use of NSAIDs cause adverse effects to the kidneys?

A

Prostaglandins control vasodilation of renal vascular beds, so inhibiton of PGs can result in decreased renal blood flow, leading to papillary necrosis

  • Risk is higher with overdose or if other risk factors are present such as preexisting renal disease, decreased renal perfusion (e.g. during anesthesia), dehydration, concurrent nephrotoxic drugs. etc.
  • Risk is higher in cats- use with caution!
47
Q

Although it is uncommon, why would the use of NSAIDs cause adverse effects to the liver?

A

Acetaminophen is metabolized to toxic intermediates by phase I metabolism in the liver, then conjugated with glutathione for excretion

  • Greater production of intermediates in cats
  • Methemoglobinemia possible as well (more common in cats)
48
Q

Besides adverse effects in the GI, kidneys, and liver, what other precautions should be taken before the use of NSAIDs?

A
  • Increased bleeding time (uncommon)
  • Agranulocytosis (uncommon)
  • Caution if any renal or hepatic disease, hypoproteinemia, late pregnancy, dehydration (hypovolemia)
49
Q

Which drug interaction with NSAIDs causes increased risk of GI irritation/ulcers?

  1. Digoxin
  2. Warfarin, anesthetics, other NSAIDs
  3. ACE inhibitors, aminoglycosides, furosemide, etc.
  4. Glucocorticoids
A
  1. Glucocorticoids
    * Contraindicated with glucocorticoid therapy
50
Q

Which drug interaction with NSAIDs causes an additive risk of renal damage/toxicity?

  1. Digoxin
  2. Warfarin, anesthetics, other NSAIDs
  3. ACE inhibitors, aminoglycosides, furosemide, etc.
  4. Glucocorticoids
A
  1. ACE inhibitors, aminoglycosides, furosemide, etc.
51
Q

Which drug interaction with NSAIDs causes drug displacement from plasma binding sites?

  1. Digoxin
  2. Warfarin, anesthetics, other NSAIDs
  3. ACE inhibitors, aminoglycosides, furosemide, etc.
  4. Glucocorticoids
A
  1. Warfarin, anesthetics, other NSAIDs
    * Contraindicated with anticoagulant therapy or if anticoagulant rodenticide toxicity
52
Q

Which drug interaction with NSAIDs causes decreased digoxin excretion?

  1. Digoxin
  2. Warfarin, anesthetics, other NSAIDs
  3. ACE inhibitors, aminoglycosides, furosemide, etc.
  4. Glucocorticoids
A
  1. Digoxin (no shit)
53
Q

This COX-1 selective NSAID is generally not used for analgesia, but most frequently used to inhibit platelet aggregation in patients prone to thrombotic disease.

  1. Firocoxib (Equioxx, Previcox)
  2. Robenacoxib (Onsior)
  3. Carprofen (Rimadyl)
  4. Meloxicam (Metacam)
  5. Derocoxib (Deramaxx)
  6. Phenylbutazone (‘Bute’)
  7. Flunixin Meglumine (Banamine)
  8. Aspirin (ASA)
A
  1. Aspirin (ASA)
  • Gomerular disease, cardiovascular disease, IMHA?
  • Cats PO every few days
  • Dogs PO SID
54
Q

Which NSAID is generally used only in large animals orally, IV, and possibly IM in swine?

  1. Firocoxib (Equioxx, Previcox)
  2. Robenacoxib (Onsior)
  3. Carprofen (Rimadyl)
  4. Meloxicam (Metacam)
  5. Derocoxib (Deramaxx)
  6. Phenylbutazone (‘Bute’)
  7. Flunixin Meglumine (Banamine)
  8. Aspirin (ASA)
A
  1. Flunixin Meglumine (Banamine)
  • Labeled only for IV use in cattle, IM in swine (IM may cause muscle necrosis)
  • DO NOT use IM in equines
  • As with other NSAIDS caution with GI, renal, hepatic, or hematologic disease
  • Anaphylaxis seen rarely after IV administration
  • Incidence of adverse effects in small animals higher than more modern NSAIDS (DON’T USE IN SMALL ANIMAL)
  • Available in combination with Florfenicol for cattle (enterotoxemia)
55
Q

Which NSAID is commonly used in horses for musculoskeletal pain, but banned in dairy cattle?

  1. Firocoxib (Equioxx, Previcox)
  2. Robenacoxib (Onsior)
  3. Carprofen (Rimadyl)
  4. Meloxicam (Metacam)
  5. Derocoxib (Deramaxx)
  6. Phenylbutazone (‘Bute’)
  7. Flunixin Meglumine (Banamine)
  8. Aspirin (ASA)
A
  1. Phenylbutazone (‘Bute)
  • Uncommonly used in small animal (better options out there)
  • Flunixin meglumine for ‘soft tissue’ pain, while this is for musculoskeletal pain
  • PO or IV, DO NOT GIVE IM/SC because it is very irritating, sloughing/necrosis can be seen
  • Intracarotid injections can cause sezures/CNS stimulation
  • As with other NSAIDs caution with GI, renal, hepatic or hematologic disease
  • Anaphylaxis seen rarely after IV administration (caution if history of allergic response)
  • Can mask lameness- withdrawal time may be required for racing animals
56
Q

Which COX-2 preferential NSAIDs are commonly used in small animal medicine as analgesics and anti-inflammatory agents?

  1. Firocoxib (Equioxx, Previcox)
  2. Robenacoxib (Onsior)
  3. Carprofen (Rimadyl)
  4. Meloxicam (Metacam)
  5. Derocoxib (Deramaxx)
  6. Phenylbutazone (‘Bute’)
  7. Flunixin Meglumine (Banamine)
  8. Aspirin (ASA)
A
  1. Carprofen (Rimadyl)
  2. Meloxicam (Metacam)
  3. Derocoxib (Deramaxx)
  • Oral (tablets, liquids, transmucosal oral spray) and injectable (SQ)
  • Meloxicam is approved for SINGLE injection use in cats
  • May be off-label use in cats
57
Q

Which COX-2 selective NSAID is available as an oral paste for horses or chewable tablets for dogs?

  1. Firocoxib (Equioxx, Previcox)
  2. Robenacoxib (Onsior)
  3. Carprofen (Rimadyl)
  4. Meloxicam (Metacam)
  5. Derocoxib (Deramaxx)
  6. Phenylbutazone (‘Bute’)
  7. Flunixin Meglumine (Banamine)
  8. Aspirin (ASA)
A
  1. Firocoxib (Equioxx, Previcox)
58
Q

Which COX-2 selective NSAID is the first NSAID approved for multiple doses in cats (SID up to 3 days)?

  1. Firocoxib (Equioxx, Previcox)
  2. Robenacoxib (Onsior)
  3. Carprofen (Rimadyl)
  4. Meloxicam (Metacam)
  5. Derocoxib (Deramaxx)
  6. Phenylbutazone (‘Bute’)
  7. Flunixin Meglumine (Banamine)
  8. Aspirin (ASA)
A
  1. Robenacoxib (Onsior)
59
Q

If Bobby, the drug rep, told you that the new drug Cockprofen was safer than Carprofen (Rimadyl), would you stock up?

A

No because no NSAID is ‘completely safe”

  • Similar risks (GI, renal, hepatic) and cautions apply
  • Generally greater COX-2 selectivity will have fewer adverse effects
  • Look carefully at testing methodologies when comparisons are made between NSAIDS
60
Q

What do you need to do if you plan on changing from an NSAID to a steroid drug?

A

Make sure you have a sufficient washout period (typically 1-2 weeks)

61
Q

What do you need to do if you plan on changing from a steroid to an NSAID?

A

You will need to wean the steroid, then have at least 1 week washout period (this will vary more than the above case)

62
Q

What do you need to do if you plan on changing between 2 different NSAIDs?

A

You should still have washout based on half-life, or use a conservative default of 1 week (to prevent GI adverse effects mainly)

63
Q

A horse came in with a musculoskeletal disease and you need to prescribe an NSAID, what’s it going to be?

A

Phenylbutazone PO or IV

64
Q

A horse came in with soft tissue pain, what NSAID are you thinking?

A

Flunixin meglumine PO or IV

65
Q

You want to prescribe a horse an NSAID that is more selective for COX-2, which one is it?

A

Firocoxib (Equioxx) oral paste

  • Equine people will also give Previcox, which is meant for dogs, because it is cheaper (chewable tablets)
66
Q

What is the only NSAID labeled for use cattle?

A

Flunixin meglumine (Banamine)

  • It is labeled for ‘control of pyrexia (fever) associated with bovine respiratory disease, endotoxemia, and acute bovine mastitis’
  • This is an area in which you will need to make decisions regarding going ‘off label’
67
Q

Which opioid is a a common post-operative drug generally used as an oral analgesic?

A

Tramadol (Ultram)

  • Weak mu agonist but also has other mechanisms:
    • Serotonin reuptake inhibitor
    • Norepinephrine reuptake inhibitor
    • Muscarinic M1 receptor antagonist
  • May lower seizure threshold, avoid in epileptic patients
  • Caution if patients on other MAOI or SSRI drugs (additive effects)
  • DEA schedule IV drug
68
Q

[FYI] What do these drugs have in common?

  • Glucosamine chondroitin (Cosequin)
  • Polysulfated glycosaminoglycans (PSGAGs) (Adequan)
  • Pentosan polysulfate (Cartrophen-Vet)
  • Omega-3 fatty acids (Dermapet)
A

They are anti-inflammatory and chondroprotective (maintains cartilage health) agents

  • Generally low toxicity (mostly adjunct), efficacy not always proven
  • Can cause a little bit of diarrhea with a high dose
69
Q

[FYI] If tramadol doesn’t work, which drug would you use that is also labeled as an antiviral drug?

A

Amantadine (Symmetrel)

  • Used to treat Parkinson’s in humans
  • It is an NMDA antagonist which is used as an adjunctive analgesic in small animals
  • Not sure about efficacy
70
Q

Which drug is sometimes used for control of neuropathic pain as an adjunctive analgesic, but have to be careful of it containing xylitol?

A

Gabapentin (Neurontin)

  • MOA involves altering calcium influx in neuronal cells
  • May cause sedation/ataxia, frequent dosing required
  • Do not use human oral liquid in dogs (contains xylitol)
  • (Antiepileptic drug add-on)
71
Q

[FYI] Which drug is usually used as an anti-emetic, but is also used as an analgesic because it inhibits substance P, altering pain signaling?

A

Maropitant citrate (Cerenia)

  • NK-1 antagonist
72
Q

T or F. Acupuncture can be used in adjunct analgesic therapy.

A

True

Pharmacology 1 choefsho (13 decks)

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