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Pharmaco > Analgesics / NSAIDs / sedatives > Flashcards

Analgesics / NSAIDs / sedatives Flashcards

1
Q

How is remifentanil metabolized

A

By non-specific esterases in blood and tissues (does not involve liver and kidneys)

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2
Q

What is the mechanism of action of local anesthetics when administered locally vs systemically (or via epidural)

A
  • Peripheral -> bind to voltage-gated Na+ channel (on intracellular side) + cause membrane expansion leading to closure of the channel -> prevent Na influx -> no depolarization - > noconduction of signal (sensory / motor)
  • Central -> at the level of the spinal cord also inhibit Ca and K-channels, inhibit substance P binding, inhibit glutamate-mediated transmission
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3
Q

What drug can increase the duration of action of lidocaine when used peripherally / as a nerve block

A

Epinephrine (causes vasoconstriction -> less systemic absorption)

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4
Q

What is the concentration (mg/mL) of bupivacaine 0.5%

A

5 mg/mL

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5
Q

What are the max doses of lidocaine and bupivacaine in dogs and cats

A

Lidocaine:
- Dogs 6-10 mg/kg
- Cats 3-5 mg/kg

Bupivacaine:
- Dogs 2 mg/kg
- Cats 1-1.5 mg/kg

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6
Q

Mechanism of actions of opioids

A
  • Binding to G-protein coupled receptors -> inhibit adenyl cyclase -> decreased cAMP -> inhibit iCa influx -> no depolarization
  • Also decrease pre-synaptic release of neurotransmitters
  • act on modulation of pain, not transduction / conduction
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7
Q

What is the effect of opioids on respiration (with mechanism)

A

Mainly respiratory depression:
- Direct depression of medullary and pontine respiratory centers
- Decreased and delayed response of chemoreceptors to CO2

Can also cause tachypnea / panting due to excitation and alteration of thermoregulation center

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8
Q

What opioids can cause histamine release

A

Morphine, meperidine, methadone
->contra-indicated in case of mast cell tumor

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9
Q

What is the opioid most / least susceptible to cause hyperthermia in cats

A
  • Most: hydromorphone
  • Least: supposed to be buprenorphine
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10
Q

What is the effect of opioid overdose on their duration of action

A

Greatly prolonged duration of action due to saturation of hepatic metabolism (conjugation)

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11
Q

What is the oral transmucosal bioavailability of buprenorphine

A

50% in both dogs and cats

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12
Q

What is the main difference between the effects of pure mu-agonists and partial mu-agonists

A

The effects of pure mu-agonists are dose dependent, the effects of partial mu-agonists have a ceiling effect after a certain dose and can never reach a maximum (thought to be more true for respiratory depression than analgesia)

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13
Q

Mechanism of action of benzodiazepines

A
  • Bind to GABA-A receptors and facilitate inhibitory function of GABA (enhances affinity of receptor for GABA)
  • Serotonin antagonists
  • Decrease release of ACh in CNS
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14
Q

Why should cats not receive diazepam CRIs

A

Diazepam is formulated in propylene glycol which can cause MetHb / Heinz body anemia especially in cats

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15
Q

What is the recommended dose for flumazenil

A

0.01-0.02 mg/kg IV

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16
Q

Where are alpha2-adrenoreceptors found

A
  • Pre-synaptic on noradrenergic neurons to give negative feedback –> inhibition of norepinephrine release
  • Post-synaptic on smooth muscle, liver, pancreas, platelets, kidney, adipose tissue, eye
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17
Q

Mechanism of action of alpha2-agonists

A

Bind to alpha2-adrenoreceptor (= Gi receptor) -> inhibition of adenyl cyclase ->decreased cAMP -> inhibition of Ca influx, enhancement of K efflux and Na/H exchange -> no depolarization -> no signal

Sedation due to effect in brainstem (corpus ceruleus) and analgesia due to effect in dorsal horn of spinal cord and brainstem

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18
Q

Explain the cardiovascular effects of alpha2-agonists

A
  • Phase I: stimulation of alpha2 receptors on vascular smooth muscle -> vasoconstriction -> hypertension -> reflex bradycardia (baroreflex)
  • Phase II: inhibition of sympathetic tone by pre-synaptic alpha2 receptors (decrease release of norepinephrine) -> bradycardia, possible arrhythmias, hypotension (once vascular resistance back to normal)
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19
Q

What is a metabolic adverse effect of alpha2-agonists

A

Inhibition of insulin and stimulation of GH -> hyperglycemia

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20
Q

What other receptors (non-adrenergic) do alpha2-agonists bind

A

Imidazoline receptors (I1 and I2) responsible for some cardiovascular, renal and metabolic effects

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21
Q

What alpha2-antagonist is supposed to only reverse peripheral (eg. cardiovascular) effects of alpha2-agonists

A

Vatinoxan (does not cross blood-brain barrier)

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22
Q

Describe the arachidonic acid cascade and indicate the mechanism of action of NSAIDs, corticosteroids, and grapiprant

A

See picture

  • Corticosteroids = phospholipase inhibitors
  • NSAIDs = COX inhibitors
  • Grapiprant = EP4 receptor inhibitor (nociception from PGH2)
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23
Q

What are the different cyclo-oxygenase (COX) enzymes and their roles

A
  1. COX-1 = constitutive -> housekeeping prostaglandins
    - gastroprotection (secretion of mucus and HCO3- + increased blood flow to gastric mucosa): PGE2, prostacyclin (PGI2)
    - renal perfusion (vasodilation of afferent +/- efferent arteriole, inhibition of Na reabsorption): PGE2, prostacyclin (PGI2)
    - hemostasis (increased platelet aggregation): thromboxane
  2. COX-2 = inducible -> most involved in inflammation, increased after tissue injury
    - Cytokines, endotoxins, growth factors ->sensitization of nociceptors
    - responsible for gastric mucosa healing mechanisms
    - anticoagulant (inhibition of platelet aggregation): prostacyclin (PGI2)
  3. COX-3 = subform of COX-1 in cerebral cortex

(some functions of COX-2 are constitutive and some functions of COX-1 also contribute to inflammation)

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24
Q

Where is COX-1 preferentially found in the body

A

Stomach, kidneys, endothelium, platelets

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25
Q

What is a risk with co-administration of NSAIDs and PPIs

A

PPIs leading to dysbiosis and predisposing to lower GI effects of NSAIDs (although protects against gastric ulcers)

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26
Q

By what mechanism are NSAIDs metabolized

A

Glucuronidation (phenolic compounds: acetaminophen, cartrofen) or oxidation (oxicam group) by cytochrome P450 in liver

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27
Q

What are the generations of NSAIDs

A
  • First generation = non-selective COX inhibitors
    Aspirin (irreversible COX inhibition), phenylbutazone
  • Second generation = non-selective COX inhibitors
    Meloxicam, Carprofen
  • Third generation (coxibs) = selective COX-2 inhibitors
    Firocoxib, Robenacoxib, Deracoxib
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28
Q

What is the difference between aspirin and other NSAIDs

A

Irreversible binding to COX complex -> irreversible inhibition of COX -> since platelets cannot synthesize new COX (no nucleus) they are inactivated for 9-11 days (lifespan)

Also cause direct injury to the gastric mucosa

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29
Q

What prostaglandin is the most associated with inflammation and nociception

A

Prostaglandin E2

30
Q

Name 2 COX-3 antagonists

A

Acetaminophen
Metamizole

31
Q

How is gabapentin eliminated

A

Renal excretion

32
Q

What is the metabolite of tramadol responsible for its opioid activity? What is the enzyme responsible for its formation

A

O-desmethyltramadol (M1)
-> found in cats but not in dogs

Enzyme CYP2D15 (a type of cytochrome P450 enzyme)

33
Q

Name some drugs known to be cytochrome P inhibitors

A
  • Azole antifungals (ketoconazole)
  • Macrolides
  • Phenothiazines
  • Chloramphenicol
  • Cannabidiol (CBD)
34
Q

Mechanism of action of trazodone

A
  • Inhibitor of serotonin transporter and serotonin type 2 receptor -> inhibition of reuptake of serotonin and changes in pre-synaptic 5-HT receptor -> 5-HT2A and 5-HT2C antagonist + increases cerebral serotonin
  • Blocks histamine H1 receptor, alpha-1 adrenergic receptor, and T-type calcium channels
35
Q

What are clinical signs of serotonin syndrome? What drugs can contribute to its development? What drug can be used to treat it?

A
  • Vomiting, diarrhea, seizures, hyperthermia, hyperesthesia, mydrasis, vocalization, hypersalivation, dyspnea, ataxia, (coma, death)
  • Metoclopramide, trazodone, tramadol, selective serotonin reuptake inhibitors (Fluoxetine), tricyclic antidepressants (amitriptyline), mirtazapine
  • Can use cyproheptadine
36
Q

What is the relative potency (compared to morphine) of methadone, hydromorphone, butorphanol, buprenorphine, fentanyl, remifentanil

A

See picture

37
Q

What is the mechanism of opioid tolerance

A

Internalization and inactivation of mu-receptors replaced by delta-receptors + NMDA up-regulation

38
Q

What protein is deficient in the MDR1 (ABCB1) mutation

A

P-glycoprotein (protein regulating transport of several drugs including opioids and acepromazine across the blood brain barrier)

39
Q

Mechanism of action of propofol

A

GABA-A agonist (potentiation of GABA induced chloride current) + NMDA inhibitor

40
Q

Mechanism of action of ketamine

A
  • Non-competitive NMDA antagonist: binds to phencyclidine‐binding and prevents glutamate binding –> dissociation of limbic and thalamocortical systems
  • Muscarinic antagonist

+ interaction with opioid receptors and monoaminergic receptors (adrenergic, serotoninergic, etc) but unclear significance

41
Q

Name 3 possible contra-indications to the use of ketamine

A
  • Cardiac disease
  • Tachycardia / hypertension / arrhythmias
  • Glaucoma
  • Patients with high ICP
42
Q

What are the 3 categories of active chemical constituents in cannabis

A
  • Phytocannabinoids
  • Terpenes and terpenoids
  • Flavonoids
43
Q

List 5 characteristics (good and bad) of propofol anesthesia

A
  • Rapid kinetics allowing titration of anesthetic depth
  • Prolonged recoveries due to increased half-time as duration of administration increases
  • Dose dependent hypoventilation and apnea
  • Vasodilation and myocardial depression
  • Risk of Heinz body anemia in cats
44
Q

What is the pathophysiology behind propofol induced Heinz body anemia?

A

Propofol leads to inhibition of erythrocyte glutathione reductase (GSH), increasing susceptibility to oxidative damage –> Heinz bodies –> increases fragility of RBCs and decreases their flexibility –> intravascular hemolysis and hemoglobinemia

45
Q

What is the mechanism of action of alfaxalone?

A

Binds GABA receptor in CNS

46
Q

Explain why cats may have slower recoveries from ketamine and in which patient population should it be avoided (for this reason in particular)?

A

In dogs, ketamine is metabolized to inactive metabolites in the liver and really excreted.

In cats, it is metabolized to norketamine (active metabolite) before being excreted in urine –> can lead to significant accumulation especially in cats with renal disease

47
Q

Why is ketamine contra-indicated in animals with increased ICP?

A

Sympathomimetic effects –> increased cerebral blood flow ICP

48
Q

True or false: Etomidate is a reasonable drug choice for maintenance anesthesia in mechanically ventilated patients.

A

False! Not recommended due adrenocortical suppression (even with a single bolus)

49
Q

Which opioid may be associated with the development of hyperalgesia?

A

Remifentanyl

50
Q

A patient receiving multimodal anesthesia (CRIs) on the MV develops lactic acidosis, hyperosmolality, hemolysis and cardiac arrhythmias. What drug could cause this and why?

A

Diazepam - propylene glycol toxicoses –> not seen with midazolam

51
Q

What is the mechanism of action of acepromazine?

A

Phenothiazine

  • Blockade of D2 dopamine receptor
  • Alpha-1 blockade –> hypotension
52
Q

What type of medication is gabapentin?

A

Calcium channel antagonist

Inhibition of alpha-2-delta-1 subunit of voltage gated calcium channels (presynaptic membrane)

53
Q

What is the mechanism of action of methadone?

A

mu-agonist + noncompetitive inhibitor of NMDA

Reduce reuptake of norepinephrine and serotonin

54
Q

Complete the sentence:
Butorphanol is a _ agonist

A

kappa

partial mu antagonist & antagonsist

55
Q

For the following drugs, list the time of onset and duration of action

  1. Propofol IV
  2. Alfaxalone IV
A
  1. 30 seconds, 5-10 minutes
  2. 60 seconds, 14-50 minutes
56
Q

List 3 cardiovascular effects of ketamine

A

Centrally mediated sympathetic response + endogenous catecholamine release:
1. Increased HR
2. Increased BP
3. Increased CO

  1. Direct myocardial depression
57
Q

List 3 effects of lidocaine

A
  1. Analgesia
  2. Antiarrhythmic
  3. Free radical scavenger
58
Q

List 3 drugs that should be avoided in animals with splenic disease and why

A
  1. Propofol
  2. Acepromazine
  3. Thiopental

–> these drugs can result in splenomegaly –> could lead to tumor rupture or hemorrhage

59
Q

Why do some mu-agonists cause hypotension when given IV too quickly?

A

They release histamine

60
Q

What is an adverse effect of bupivacaine?

A

Arrhythmias and reduced CO

61
Q

List at least 5 physiologic effects of opioids (other than analgesia) and why they occur

A
  • Excitatory response –> activation of dopaminergic receptors in the hypothalamus
  • Respiratory depression –> depression of pontine and medullary respiratory centres + delayed and decreased response to arterial CO2
  • Tachypnea –> excitation and/or alteration of thermoregulatory centre
  • Hypo/hyperthermia –> alteration of thermoregulatory centre
  • Bradycardia –> Vaguely mediated (or pain relief)
  • Hypotension –> histamine release (only morphine, methadone meperidine)
62
Q

Why are morphine & methadone contra-indicated in patients with mast-cell tumours?

A

Can cause release of histamine

63
Q

Why do anesthesiologists get mad at us if a patient has received buprenorphine prior to GA :)

A

Buprenorphine binds with great affinity to the receptors and is difficult to reverse.

Dissociates slowly from mu receptors

64
Q

3 regions of the CNS where benzodiazepines act

A

Limbic
Thalamic
Hypothalamic

65
Q

What route of diazepam administration has been associated with idiosyncratic hepatic failure in cats?

A

PO

66
Q

List 3 differences between midazolam and diazepam

A
  • Diazepam is not water soluble
  • Diazepam is formulated with propylene glycol
  • Midazolam is poorly available when given rectally
  • Midazolam is shorter acting (short half-life)
67
Q

List 3 drug interactions with alpha2-gonists that may improve analgesia

A
  • Potentiation of opioid induced analgesia
  • Decreased development of opioid tolerance
  • Synergistic analgesic effect with NSAIDs and acetaminophen
68
Q

What can happen if atipamezole is given IV?

A

Transient but sometimes severe dysphoria

69
Q

Why are cats more sensitive to acetaminophen?

A

They have deficient glucuronidation (essential for NSAID metabolism via P-450)

70
Q

True or false: acetaminophen cannot be given with NSAIDs

A

False

71
Q

Explain NSAID induced lower GI toxicity

A

Enterohepatic recycling –> prolonged and repeated exposure of the intestinal mucosa to the drug and its compounds

Independent of acid secretion

Pharmaco (7 decks)

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