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VM722 Pharm > Exam 3 Hellyer > Flashcards

Exam 3 Hellyer Flashcards

1
Q

What are primary reasons NSAIDs are used in animals

A

Anti-inflammatory, analgesia, antipyretic

acute pain, chronic musculoskeletal disorders

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2
Q

Most common complication/side effect of NSAIDs in the dog

A

GI problems - gastritis, enteritis, ulceration, inappetence, vomiting, bloody diarrhea

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3
Q

What organ system is most concerning when giving an NSAID to an adult cat?

A

Renal

NSAID’s decrease PG’s –> decreased renal perfusion

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4
Q

What can you give with an NSAID to enhance post-op analgesia?

A

opioids like Tramadol or buprenorphine

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5
Q

What is grapiprant?

A

NSAID that doesn’t inhibit cox, instead highly selective for PG-E2/EP4 receptor, and more mild side effects

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6
Q

What are the two main opiate receptors that are targeted clinically?

A

Mu & Kappa

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7
Q

What is a full mu agonist?

A

Opioid that binds completely causing a maximal response /stim of the receptors (aka max analgesia)
e.g. Morphine

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8
Q

What is a partial mu agonist?

A

Binds to mu receptor but doesn’t fully activate it –> lessened analgesic effects
E.g. buprenorphine (less effective but higher affinity for mu receptor than morphine, will outcompete)

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9
Q

What is an opioid agonist-antagonist?

A

Antaognist effect at one receptor (mu) but also has agonist effect other receptor (kappa)
More potent sedative, less use as an analgesic
or would decrease analgesic effect if given after morphine
E.g. butorphanol

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10
Q

What is naloxone, how does it work?

A

Full antagonist - blocks both mu & kappa receptors

Reversal for buprenorphine, opioids

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11
Q

Which opioid is difficult to reverse due to high binding affinity?

A

Buprenorphine - easily displaces full agonists on mu receptors

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12
Q

Butorphanol vs. Fentanyl for respiratory depressant effects

A

Both cause respiratory depression, but spp differences for sensitivity to each drug
Brachiocephalics/frenchies more sensitive - ceiling effect on resp depression w/ butorphanol vs. fentanyl

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13
Q

How could you treat opioid-induced excitement in a dog?

A
  1. Reverse the opioid
  2. Give naloxone if you don’t want them to lose analgesia or if they can’t tolerate more opiods
  3. Could give sedative - acepromazine or Dexmedatomadine
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14
Q

Convenient and effective way for clients to give buprenorphine in a cat?

A

Transmucosally (rub on cheeks)

90% bioavailability

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15
Q

Anesthetized dog’s HR drops from 100 to 40 bpm after IV administration of Fentanyl. What can you do?

A

Give atropine/glycopyrrolate (anticholinergic) to maintain analgesia but increase HR

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16
Q

How would you completely reverse the effect of hydromorphone?

A

Naloxone

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17
Q

How would you completely reverse the effect of butorphanol?

A

Naloxone

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18
Q

How would you completely reverse the effect of buprenorphine?

A

With time.

Could try Naloxone, probably won’t work and would have to be very high dose.

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19
Q

What is the MOA for Diazepam?

A

Enhances the effect of GABA - keeps the chlorid ion channels open longer, cell membrane is more hyperpolzarized –> decreased frequency of AP’s, inhibitory to CNS

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20
Q

How effective of a sedative is Diazepam in young, healthy animals?

A

Minimal to no calming in young, healthy animals
Some will sedate, some will get wierd. not really effective.
(but profound calming in sick, compromised animals)

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21
Q

How do Diazepam and Midazolam differ?

A

D - insoluble in water, unpredictable absorption, long lasting, stings b/c mixed in propylene glycol base, metabolites eliminated in kidneys
M - water soluble, rapid absorption & more potent than D, short lasting, metabolites are inactive

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22
Q

When would it be appropriate to administers flumazenil?

A
  • Reversal/antagonist for benzodiazepines (Diazepam, Midazolam)
  • to make a more smooth recovery, reduce action of sedatives/tranquilizers
  • DONT administer if hx of seizures
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23
Q

What is the primary use for acepromazine?

A

Depresses hypothalamus and RAS = tranquilizer

Patient awake but calm, relaxed

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24
Q

How are acepormazine effects antagonized?

A

No antagonist available (b/c works on lots of receptor types, broad effects) but patient can override drug effects w/ sufficient stim

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25
Q

What are the effects of Acepromazine on the cardiovascular system?

A
  • vasodilation (primary effect), which can –> hypotension (esp. during anesthesia)
  • may see reflex tachycardia
26
Q

How can you enhance the sedative effects of acepromazine in dogs/cats?

A
  • give concurrently with opioids or alpha 2 agonists
  • decreases amount of drugs needed for sedation
  • lower dose can lessen vasodilation
27
Q

What are the primary uses of trazodone?

A
  • Anxiolytic (anti-anxiety) for behavioral issues

- used as pre-treatment for anxious dogs coming into clinic

28
Q

What are the desirable effects of alpha-2 agonists?

A
  • muscle relaxation (via CNS inhbition)
  • sedation (can be enhanced if given w/ opioid)
  • analgesic (w/ opioid) = profound for visceral pain (Acepromazine doesn’t do)
29
Q

Effects of alpha-2 agonists on the cardiovascular system (Xylazine, dexmetatomadine)

A

HYPERtension due to vasoconstriction (dose dependent) –> hypotension only in some circumstances
Bradycardia, bradyarrhythmias, decreased CO

30
Q

Effects of alpha-2 agonists on the respiratory system

A

mild/mod resp depression (due to CNS depression)

stridor, dypsnea in EQ, brachiocephalics

31
Q

How can you antagonize effects of Demedetomidine?

A

Atipamezole (most specific alpha-2 antaognists)

or Yohimbine, Tolazoline

32
Q

How is ketamine fundamentally different from thiopental, alfaxalone, or propofol in anesthesia induction?

A
  • Causes less apnea or hypoventilation
  • Dissociative & cataleptic anesthetic (neuro fixed postures + unaware of surroundings)
  • Non-uniform depression of CNS & slower onset
33
Q

What effect does Alfaxalone have on the respiratory system?

A

resp depression, hypoventilation, could –> apnea
(plan do use assisted ventilation)
high enough dose/rapid bolus = stops breathing
Dogs - could see resp acidosis, histamine release

34
Q

What are the respiratory effects of Propofol?

A
  • Basically same as alfaxalone (resp depression, hypoventilation, could –> apnea)
  • give slowly to avoid resp issues
35
Q

What are the respiratory effects of Ketamine?

A
  • less apnea/hypoventilation than propofol/thiopental
  • Patient likely to continue to breathe on induction
  • Used in combo w/ diazepam
36
Q

What are the cardiovascular effects of Ketamine?

A

Increased sympathetic stimulation (increased HR), variable change in CO
BP often maintained or increased

37
Q

How does Ketamine increase HR and BP?

A
  • INDIRECTLY increases HR/BP via sympathetic stim
  • In really sick animals (w/ ceiling effect, symp stim tapped out) see DIRECT negative effect on heart fx (depression, decreased CO, HR
38
Q

What are the cardiovascular effects of Propofol?

A
  • Vasodilation, hypotension (can be transient or long-acting depending on dose)
  • may lead to reflex tachycardia
  • lowers BP (vs. Ketamine increases BP)
39
Q

Why would you not use Ketamine to induce anesthesia for an animal w/ head trauma?

A

It increases intracranial pressure by increasing cerebral blood flow/symp ton/BP –> ischemia, worsened neuro probs etc.

40
Q

Why is anesthesia recovery from propofol so rapid in dogs?

A
  • rapidly cleared by liver (even when dz’d)
  • AND also metabolized extrahepatically in the lungs
  • good choice for portosystemic shunt - still will be cleared safely
41
Q

What is the effect of liver dz and recovering from Propofol?

A

Recovery not as severe/long b/c of extrahepatic metabolism & rapid hepatic metabolism

42
Q

How does a prolonged infusion of propofol affect recovery in cats?

A

Longer recovery time.
Cats lack glucuronidation (lack glucuronide synthetase)
= Drug half-life longer (esp. w/ repeat boluses or infusions)

43
Q

What are the cardiovascular effects of alfaxalone?

A

Decreased CO, MAP, vasodilation, contractility

Similar or less effecitve tha propofol (debated)

44
Q

What temporary endocrine abnormality is induced by etomidate?

A

Hypoadrenocorticism for several hours. (= no stress response)
Problematic if used for long time

45
Q

Which anesthetic induction drug should be used cautiously in patients with glaucoma?

A

Ketamine - increases intraocular pressure (causes extraocular mm. contraction, elevated BP)

46
Q

How do you avoid rough, prolonged recoveries from Ketamine?

A
  • Give a tranqulizer, sedative, and analgesic
  • or combine w/ other drugs to give a lower dose + give fluids for clearance (esp. cats)
  • no reversal for Ketamine
47
Q

What is the relationship between anesthetic potency and lipid solubility?

A

the more lipid soluble, the more potent

48
Q

What are the effects of inhalant anesthetics on heart function

A
  • profound cardiac depression (esp. if more debilitated animal)
  • reduced CO, contractility, vasodilation, hypotension, decreased symp tone
49
Q

Why is the vapor pressure of the inhalant anesthetics important?

A

It determines the type of calibrated vaporizer required to ensure safe delivery of inhalant to the patient

50
Q

How does blood:gas solubility of an inhalant affect the rate of change of anesthesia?

A

Determines how rapidly an anesthetic saturates blood & induced general anesthesia (b/c moves along conc gradients)

  • less soluble = anesthesia induced faster (b/c blood takes up more before saturated)
  • more soluble = longer before anesthetic effect seen & longer recovery time
51
Q

What decreases MAC (minimum alveolar concentration needed to induce anesthesia in 50% of patients)

A

-Pre-med with other agents (e.g. opioids, acepro, alpha 2, ketamine, propofol, etc)
- Hypothermia
Lower MAC = less anesthesia required to stay under, less inhalant needed to maintain anesthesia

52
Q

What are the effects of inhalants on cardiovascular function?

A

Decreased CO, contractility,
Vasodilation, hypotension
May cause arrhythmias
depressed symp outflow

53
Q

What are the effects of inhalants on resp function?

A

Depress resp fx (why give w/ oxygen not room air)

resp rate ma increased or decrease –> decreased minute ventilation

54
Q

MOA of local anesthetics?

A

Na channel blockers - stabilize membranes, keeping Na channels in inactivated state –> AP’s inhibited

55
Q

What is the effect of inflammation on lidocaine efficacy?

A

Efficacy decreased due to low tissue pH
Uncharged form dissociates to cross membrane, but when Inflammation occurring, lots of H+ present, anesthetic prevented from moving to cytoplasm & having an action

56
Q

What nerve fiber type is likely to be affected first with a local anesthetic?

A

First, sympathetic post-ganglionic, C-fibers (pain), pre-ganglionic autonomic - b/c small, unmyelinated
Then, delta (pain) fibers
Next, gamma fibers (muscle spindles), beta fibers (touch/pressure)
Last, alpha fibers (proprioception, somatic motor)

57
Q

Is bupivicaine or lidocaine a more toxic drug?

A

Bupivacaine more toxic - longer lasting, can’t be reversed, can cause cardiac arrest

58
Q

Clinical signs of lidocaine toxicity

A
  • CNS (first) and cardiovascular dysfunc (vs. bupivicaine they happen at same time)
  • muscle twitch, seizure, depression, comma, resp arrest
    decreased contractility, CO
  • systemic hypotension, may lead to cardiac arrest
59
Q

Treat lidocaine toxicity

A

Supportive care - will resolve with time

Diazepam/Midazolam, supp oxygen, intubate, intermittent mechanical ventilation if needed, etc.

60
Q

How does systemic administration of lidocaine produce analgesia?

A

MOA unknown, likely due to Na/K, NMDA receptor inhibition, inhibition of glycine uptake

use for ventricular arrhythmias

61
Q

What is Nocita, how does it differ from bupivacaine?

A

Liposome injectable suspension of Bupivicane

Formulated to stay where you put it and cause slow release of bupivicaine

VM722 Pharm (5 decks)

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