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RUSVM Pharmacology > Analgesics- Local and NSAIDs > Flashcards

Analgesics- Local and NSAIDs Flashcards

1
Q

The detection of a noxious stimulus at the tissue

A

Nociception

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2
Q

Free nerve endings of primary afferent neurons that detect noxious stimuli

A

Nociceptors

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3
Q

What are the 5 processes that play a role in nocicpetion

A 
Transduction -> stimuli to AP
Transmission -> peripheral nerves to CNS
Modulation ->dorsal horn of spinal cord 
Projection ->2nd order to thalamus 
Perception -> integration
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4
Q

What are the types of primary sensory nocicpetion nerve fibers

A

AB fibers
A-delta (pinpoint; mechanical/thermal)
C-fibers (diffuse; many stimuli )

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5
Q

Pain that persists longer than it is providing protection

A

Chronic pain

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6
Q

Exaggerated perception of pain produced by a noxious stimuli

A

Hyperalgesia

Primary-> occurs in area of tissue damage
Secondary-> occurs beyond region of injury

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7
Q

non-noxious stimuli that elicits pain

A

Allodynia

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8
Q

________________ activate nociceptors

A

Inflammatory mediators

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9
Q

Pain receptor change from high to low threshold

A

Primary hyperalgesia

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10
Q

Inflammatory mediators activate more nociceptors adjacent to injury

A

Secondary hyperalgesia

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11
Q

Where does central pain sensitization occur and what receptors are involved

A

Dorsal horn of the spinal cord

NMDA receptors

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12
Q

What is pain sensitization

A

Changes occur in sensory processing enabling low intensity stimuli to produce pain.

NMDA and Glutamate - increase in excitatory neurotransmitters cause hyper-excitability in dorsal horn neuron

Occurs in acute and chronic pain

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13
Q

What receptor plays a central role in chronic pain

A

NMDA receptor

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14
Q

What is the main effect of local anesthetic?

A

Reversible blockade of transmission

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15
Q

What drugs can be used for local anesthesia

A 
Lidocaine 
Bupivicaine 
Mepivicaine 
Ropivicaine
Proparacaine 
Procaine
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16
Q

Local anesthetics belong to what two chemical groups

A

Amides

Esters

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17
Q

Are local anesthetics weak bases or acids?

A

Weak bases

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18
Q

What are the amide local anesthetics ?

A

Lidocaine
Bupivacaine
Mepivacaine

Metabolized in the liver

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19
Q

What are the ester local anesthetics

A

Procaine
Proparacaine

Hydrolyzed by plasma esterases

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20
Q

What is the MOA of local anesthetics?

A

Cross lipid membrane of nerve cell into the cytoplasm

Prevent depolarization and block the propagation of an action potential by inhibiting the influx of sodium

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21
Q

What is the onset of blockade of local anesthetics??

A

Small. Myelinated A-delta fibers (sensory)
Unmyelinated C fibers (sensory/autonomic)
Large myelinated Aa fibers(motor)

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22
Q

The effect of local anesthetic is usually terminated by ____________

A

Redistribution

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23
Q

Why would you use epinephrine in conjunction with a local anesthetic

A

Epinephrine causes vasoconstriction which decreases the distribution of the anesthetic from its site of action => longer lasting effect

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24
Q

The duration of a local anesthetic will be affected by?

A

Lipophilicity

Ability to bind sodium channel

Underlying disease -> hepatic disease=increased duration of amides

Drug-drug interaction

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25
Q

Esters are broken down by?

A

Plasma esterases

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26
Q

Where are amides metabolized

A

Liver

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27
Q

Where are local anesthetic metabolites excreted

A

Urine

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28
Q

How does the half life of esters compare to amide local anesthetics?

A

Esters- few minutes; rapidly broken down by plasma cholinestersase

Amides- hours (2-6); metabolized in the liver

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29
Q

Increasing the _______________ of urine will increase local anesthetic elimination

A

Acidity

Local anesthetics are all weak bases

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30
Q

What routes of administration can be used for local anesthetics?

A

Topical - skin/wound/splash block

Local infiltration -peripheral nerve block/intra-aricular/epidural

Intravenous -Bier’s block

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31
Q

What are the clinical uses of local anesthetics?

A

Regional anesthesia
Pre and post-operative analgesia
Wound management
Peri-operative analgesia

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32
Q

When is regional anesthesia used?

A

Minor procedures
Lameness localization
Epidural

-completely block nociception at site of injury or surgery

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33
Q

What kind of regional analgesia can be used for injury/surgery distal to the elbow

A

Brachial plexus block

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34
Q

What kind of regional analgesia could be used for thoracotomy, chest tube, or rib fractures

A

Intercostal nerve block

Injections -> three ribs anterior and two ribs posterior to site of injury

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35
Q

What are the benefits to regional analgesia ?

A 
Less sedation 
Decreased nausea and vomiting 
Decreased CV and pulmonary complications 
Shorter hospitalization 
Decreased infection 
Decreased morbidity and mortality
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36
Q

What are the major risks of using regional analgesia?

A

Local anesthetic toxicity

Nerve injury
-trauma, toxicity, ischemia, or combination ->result from needle, intraneural injection, compression, or stretch

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37
Q

What are the contraindications to using epidurals

A

Coagulopathy
Anatomy
Skin infection/ sepsis
Neurological disease

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38
Q

What are the complications that can arise from an epidural

A 
Horners
Hypotension 
Hypoventilation 
Schiff-Sherrington 
Muscle twitching 
Hypoglycemia 
Urinary retention
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39
Q

What is the most commonly used local anesthetic in vet med

40
Q

What is the onset of action and duration of lidocaine?

A

Rapid onset -5mins

Duration -40-60mins

41
Q

Lidocaine is metabolized where

42
Q

What animals are sensitive to lidocaine

A

Do not exceed 4-7mg/kg

Cats more than dogs
Sheep may be more sensitive than other livestock

43
Q

_______________ is used as a topical gel/ointment for dermal analgesia

A

5% ELMA cream (2.5%lidocaine / 2.5% prilocaine)

44
Q

What is a lidocaine solution for injection

A

Lidocaine (Xylocaine) -local use

45
Q

What are the clinical uses of lidocaine?

A 
Systemic 
Antiarrhythic (IV)- class 1B antiarrhythmic- control arrhythmias

Preanesthetic (IV)

Analgesic with anti-inflammatory properties

Antioxidant

GI prokinestic -increase GI motility in horses

46
Q

What is the most cardiotoxic of the local anesthetics?

A

Bupivacaine

47
Q

Local anesthetic that is infused through thoracostomy tubes or wound soaker catheters

A

Bupivacaine

48
Q

What is a precaution to using Bupivacaine?

A

Cardiotoxic
->Should not used in patients post pericardectomy

Phrenic nerve paresis or paralysis

49
Q

Why do cats generally have lower dose of analgesics than dogs?

A

Cats are deficient in hepatic metabolism
Sensitive to anesthetics

Amides are degraded in the liverr

50
Q

What is the drug of choice for diagnostic nerve blocks in horses

A

Mepivacaine

51
Q

How does the duration of action differ between the amide anesthetics?

A

Lidocaine < Mepivicaine < Bupivicaine

52
Q

What local anesthetic is used topically for corneal and conjunctival manipulation

A

Proparacaine

53
Q

What is the onset and duration of proparacaine?

A 
Rapid (30sec)
Short duration (10-20mins)
54
Q

What are the contraindications to proparacaine use?

A

Long term corneal use –> toxic

55
Q

What ester anesthetic is a class 1a antiarrhythmic

A

Procainamide

56
Q

What ester analgesic is not used as a local anesthetic but is present in some Penicillin G preparations

57
Q

What ester analgesic is VERY toxic to cats and can cause Heinz body anemia and blood dyscrasia

A

Benzocaine

58
Q

What nociception process is least affected by the administration of local anesthetic drugs ?

A

Perception

Projection

59
Q

What two nocicpetion processes are affected by NSAIDs ?

A

Transduction and modulation

60
Q

What is the main effect of NSAID

A

Inhibiting cyclooxygenase (COX) enzymes

61
Q

What is the role of COX1 enzyme

A

Production of prostaglandins
Mediates Thromboxane A2 -> platelet aggregation
Prostaglandin E1 -> maintain GI mucosa

62
Q

What is the role of COX2

A

Production of prostaglandin in times of inflammation

63
Q

what are the COX2 selective inhibiton NSAID

A 
Carprofen 
Derocoxib 
Robenacoxib 
Firocoxib 
Meloxicam 
Piroxicam
64
Q

What are the non-selective COX1 and COX2 inhibitors

A

Phenylbutazone

Flunixin meglumine

65
Q

What is a selective COX1 inhibitor

66
Q

T/F: NSAID are all weak bases

A

F

Weak acids

67
Q

What are the 4 effects of NSAIDs

A

Anti-inflammatory -> inhibit eicosanoids synthesis (thromboxane, prostacyclin, and prostaglandin)

Analgesic -> decrease PG sensitization of neurons

Antipyretic -> reduce fever

Antiendotoxic (if given before endotoxic challenge)

68
Q

What is the strongest acid of NSAIDs

A

Aspirin ->salicylic acid

69
Q

What is a COX1 selective inhibitor

70
Q

What are the non specific COX inhibitors

A

Flunixin
Phenylbutazone
Ketoprofen

71
Q

What are the COX2 preferential inhibitors

A

Deracoxib
Carprofen
Meloxicam

72
Q

What are the COX2 selective inhibitors

A

Firocoxib

Robenacoxib

73
Q

T/F: NSAIDs can cross the BBB

74
Q

Where does NSAID metabolism take place and how are NSAIDs excreted?

A

Liver

Urine and Biliary excretion (some NSAIDS have enterohepatic recirculation)

75
Q

Antithrombotic effect of NSAID?

A

Inhibits thromboxane A2 -> no platelet aggregation

76
Q

What are the antineoplastic effects of NSAIDs

A

COX2 is expressed by some cancers

Eg Transitional cell carcinoma
Osteoscarcoma

77
Q

What NSAID is used often for its antineoplastic effects?

78
Q

What are the adverse effects of using NSAIDs

A

GI irritation/ ulceration -> prostaglandins maintain GI homeostasis

Renal damage and decreased blood flow -> PG control vasodilation –> decrease renal flow and papillary necrosis

Post operative analgesia and hypotension

Hepatotoxicity (acetaminophen metabolized to toxic intermediate)

79
Q

What species is at a higher risk of renal damage from NSAIDs?

80
Q

What drug is commonly used for colic/visceral pain in horses/cattle?

A

Flunixin Meglumine

81
Q

What is the proper route of administration of Flunixin Meglumine

A

PO, IV, IM

Do NOT give IM to horse -> muscle necrosis

82
Q

What species should you avoid using Flunixin Meglumine in due to its renal toxicity in

83
Q

What drug is commonly used in horses to treat musculoskeletal pain

A

Phenylbutazone

84
Q

What are the route of admin for Phenylbutazone

85
Q

What is a washout period and when should you use one

A

Period, based on half life, that it takes for a drug to leave the system (usually 1-2wks)

Changing from steroid to NSAID
Changing from two different NSAIDs

86
Q

What is the MOA of acetaminophen

A

Interferes with convertibility endoperoxides to PG and TX

87
Q

When is acetaminophen used clinically?

A

Dogs -sometimes after neurological surgery

NEVER in cats

88
Q

What are the toxic effects of Acetaminophen ?

A

Methemoglobinemia->MOST important
Hepatic necrosis

Hemolysis, icterus, anemia, Heinz bodies

Facial swelling, edema

89
Q

What non-NSAID is an antagonist at prostaglandin E2 (PGE2) EP4 receptor

A

Grapiprant what

90
Q

What is used to control neuropathic pain and prevent allodynia in dogs, cats, and horses

A

Gabapentin

Pre-emptively for acute pain or treat laminitis

91
Q

What are the precautions to using Gabapentin

A

Sedation/ataxia ->dose dependent effects

Renally excreted-> caution in renal insufficiency

92
Q

What is used to treat neuropathic pain or dorsal horn “windup” pain

A

Amantadine

Less common in small Amina’s

93
Q

What is the MOA of Amantidine

A

Antiviral with NMDA receptor antagonist

94
Q 
Which of the following drugs is NOT a selective COX2 inhibitor ?
A. Carprofen 
B. Phenylbutazone 
C. Robenacoxib 
D. Meloxicam
A

B. Phenylbutazone

95
Q

What is the mechanism of action for the antithrombotic effects of aspirin

A

Irreversible thromboxane A2 inhibition

Binds to thromboxane receptor on platelet for the lifespan of the receptor (8-10days)

96
Q

Why is IM injection of flunixin meglumine contraindicated in horses?

A

Risk of muscle necrosis

97
Q

Do you use NSAIDs with glucocorticoids

A

NO! ARE YOU INSANE!?!?!?

RUSVM Pharmacology (18 decks)

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