Anesthesia & pain management Flashcards

1
Q

What steps should we follow as part of a check list for every patient to decrease errors and increase patient safety?

A
  1. Preanesthetic evaluation and patient considerations -> history, age, breed…
  2. Considerations prior to coming to the clinic -> fasting, other medications, patient experience motion sickness, anxiolytic drugs…
  3. Equipment preparation -> decide circuit, check anesthesia machine, ensure all equipment works.
  4. Patient preparation -> accurate weight, stabilization
  5. Anesthetic protocol -> pain management, local blocks. Premedication, induction, maintenance -> multimodal approach.
  6. Monitoring during anesthesia -> physiologic monitoring and support (O2, fluids)
  7. Troubleshoot anesthetic complications -> cardiovascular (hypo/hypertension, arrhythmias, achy/bradycardia), respiratory (hypoventilation, hypoxemia), other (hypothermia, regurgitation)
  8. Recovery from anesthesia -> most deaths occur here!!
  9. Patient returns home -> consider at home analgesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Preanesthetic evaluation and plan considerations include the following

A
History
Physical exam
Age
Breed / Size
Temperament
Patient diagnosis
Other: type of procedure (level of invasion, pain management), clinical staff training, time of the day.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the recommendations on fasting prior to an anesthetic event based on the AAHA 2020 guidelines?

A
  • In general, the recommended fast duration for healthy adult patients has decreased. The change is based on clinical experience and experimental evidence of shorter fasting benefits, including a lower incidence of GER. An abbreviated fast is particularly important for diabetic and neonatal patients.
  • Healthy adults -> withhold food for 4-6h. No water restriction.
  • <8w of age of <2kg -> withhold food for no longer than 1-2h. No water restriction.
  • Diabetics -> withhold food for 2-4h. No water restriction.
  • Hx or at risk of regurgitation -> withhold food AND water for 6-12h.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ASA patient classification

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Risk of death by ASA status

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Recommendations for chronic medications the day of anesthesia - continue as scheduled

A

· Thyroid medication: thyroid supplement or methimazole
· Behavioral and analgesic medications: sudden withdrawal of these medications is not advised
· Oral anxiolytics: to reduce fear and anxiety
· Cardiac medications: pimobendan, furosemide
· Antibiotics
· Steroids: should not be abruptly stopped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Recommendations for chronic medications the day of anesthesia - discontinue the day of anesthesia

A
  • Antihypertensive medication, especially ACE inhibitors: enalapril, benazepril
  • Anticoagulants: may need to be discontinued 2 wk prior to anesthesia based on risk of bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Recommendations for chronic medications the day of anesthesia - administer based on specific instructions to the owner

A

Insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Canine or feline sacrococcygeal or coccygeal epidural procedure

A

INDICATIONS: Canine and feline tail amputations, perineal urethrostomies, anal sacculectomies, catheterization for relief of urethral obstruction, perineal relaxation for delivery of puppies/kittens, and other surgeries of the penis or perineal region.

PROCEDURE:

  1. For either dogs or cats, use 0.1 mL/kg of either lidocaine, bupivacaine, mepivacaine, or ropivacaine.
    a. A dose of 0.1 mL/kg is usually sufficient but up to 0.2 mL/kg is reported. The average volume in a cat or small dog is 0.5 mL.b. Dosing volumes are based on the following drug concentrations: lidocaine 2%, mepivacaine 2%, bupivacaine 0.5%, and ropivacaine 0.5%. If the drug concentrations used are higher, using a lower volume of the drug and diluting it with saline is recommended to ensure a safe dose at an adequate volume.
  2. To find the sacrococcygeal site, move the tail up and down in a “pumping” motion while palpating the sacrococcygeal region of the patient.
    a. The first movable space at the caudal end of the sacrum is either the sacrococcygeal or intercoccygeal space. Either site is appropriate for injection and there is no need to differentiate what site is being palpated.
  3. Insert a 25- or 22-gauge hypodermic needle through the skin ON MIDLINE at a ~45° angle to the skin surface. Proceed slowly until the needle enters the space.
    a. If bone is encountered (it usually is), withdraw the needle a few millimeters, redirect slightly (steeper or flatter angle), and reinsert (“walking” off he bone).b. Repeat this process until the needle is inserted between the vertebrae to enter the intervertebral space. A “pop” may be felt and there should be no resistance to injection.

CONSIDERATIONS:
- Pelvic limb motor function is not blocked unless the volume of local anesthetic is large, causing cranial spread to the motor nerves of the pelvic limbs. Stay at or below the 0.2 mL/kg volume.

  • If tail/anus relaxation does not occur within 5 min (within 8–10 min with bupivacaine or ropivacaine), the injection may have been made subcutaneously. Try again!
  • Opioids could be added as adjunct for perineural blocks, but they will not reach the receptors in the spinal cord and thus will not provide the long duration achieved with lumbosacral injection.
  • There is generally no need for the saline test dose as is used for lumbosacral epidurals—just inject the drugs. Do not inject air; an air bubble may cause incomplete block because this is a very small space.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Complete, regarding the process of nociception:

  1. The first step is _________ of the noxious stimulus into an electrical stimulus (_________) occurs in a discrete set of receptors (_____________)
  2. Second step is ______________ of the nervous impulse that occurs along the primary afferent fibers (_______________) from the periphery through the spinal cord and ascending relay neurons in the thalamus to the somatosensory cortex.
  3. As the signal travels through the ____________ of the spinal cord, ________________ of the message helps determine the strength of the signal reaching higher centers in the brain.
  4. projections to the reticular formation and hypothalamus increase alertness and autonomic fun
    ctions and increase _________and ______________ release
  5. Finally, integration of the aforementioned processes with the unique psychology of the individual results in the final experience of ___________
A
  1. First, transduction of the noxious stimulus into an electrical stimulus (action potential) occurs in a discrete set of receptors (nociceptors)
  2. transmission of the nervous impulse occurs along the primary afferent fibers/nerves (A-delta, A-beta and C-polymodal fibers) from the periphery through the spinal cord and ascending relay neurons in the thalamus to the somatosensory cortex.
  3. As the signal travels through the dorsal horn of the spinal cord, modulation (amplification or inhibition) of the message helps determine the strength of the signal reaching higher centers in the brain
  4. projections to the reticular formation and hypo- thalamus increase alertness and autonomic functions (e.g., heart rate and respiratory rate) and increase catecholamine and glucocorticoid release.
  5. Finally, integration of the aforementioned processes with the unique psychology of the individual results in the final experience of pain perception
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

The pharmacology of analgesics is different in patients with
chronic pain and those with acute pain. Opioid use rapidly (within hours) leads to the development of ______________and____________, both of which may be attenuated by the addition of_________ or ___________

A

opioid tolerance and opioid-induced hyperalgesia

N-methyl-d-aspartate receptor antagonist (e.g., ketamine or metha- done) or gabapentin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The ______________________is among the most completely validated multidimensional pain scale system for use in dogs with acute postoperative pain.

A

The Glasgow Composite Measures Pain Scale is among the most

completely validated multidimensional pain scale system for use in dogs with acute postoperative pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What’s the difference between allodynia and hyperalgesia

A

Allodynia –> painful response to things that don’t usually cause pain
Hyperalgesia –> exagerated response to painful stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which are the three neurons involve in the 3 neuron pathway of nociception

A
  1. Primary afferent neuron
  2. Projection neuron
  3. Supraspinal neuron
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the characteristics of visceral pain (localization, mechanism of activation, characteristics, sources of pain)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the characteristics of somatic pain (localization, mechanism of activation, characteristics, sources of pain)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the characteristics of neuropathic pain (localization, mechanism of activation, characteristics, sources of pain)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the characteristics of psycogenic pain (localization, mechanism of activation, characteristics, sources of pain)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What’s the difference between cytokines and chemokines

A

Cytokines are a broad and loose category of small proteins (~5–25 kDa) important in cell signaling.

Chemokines –> any of a class of cytokines with functions that include attracting white blood cells to sites of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

These primary afferent nerves are activated by mechanical and thermal injury and produce a short-lasting, picking-type pain

A

A-delta nociceptors –> they are the smallest myelinated nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

These primary afferent nerves are unmyelinated, having a slow conduction velocity. They produce a dull, poorly localized, burning type pain

A

C Nociceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

List the three endogenous mechanisms of pain modulation

A
  1. Descending inhibitory nerve system
  2. Endogenous opioid system
  3. Segmental inhibition or “gate control theory”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

The main transmitters involved in the descending inhibitory nerve system are:

A

Serotonin and norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Enkephalins, Endorphines and Dynorphins are part of the:

A

Main groups of endogenous compounds of the endogenous opioid system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Fill the empty boxes with any of the following options (can pick more than one and repeat the options in different boxes):
- opioids, apha- agonists, local anesthetics, NSAIDs, ketamine, general anesthethics

A

Opioids –> are found on synaptic membranes where they regulate the transmission of information from primary sensory pain afferents. Opioids also block the release of sub- stance P, an important neurotransmitter of painful stimuli, in the dorsal horn of the spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which opioid receptor would go with each of these endogenous ligands:

B- endorphin –> _____________
Leucine and methionine-enkephalin –> _______________
Dynorphin-A –> ____________________

A

Mu
Kappa
Delta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Opioids -> receptors and adverse effects

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Ketamine, dexmedetomidine, lidocaine and maropitant -> receptor and adverse effects

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Amantadine, pregabalin, gabapentin, tramadol and NSAIDs - receptor and adverse effects

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Histamine release with subsequent vasodilation and hypotension (especially if higher doses are given intravenously) may occur after giving this opioid

A

Morphine or meperidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which of these has less incidence of nausea and vomiting?

Morphine, hydromorphine and oxymorphone

A

The incidence of nausea and vomiting, a risk factor for the development of aspiration pneumonia, is less after oxymorphone (33%) than after hydromorphone (44% to 66%) or morphine (50% to 75%).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Why phenothiazined are avoided in patient with questionable cardiovascular stability

A

They act as α antagonists, causing peripheral vasodilation and possible hypotension in hypovolemic patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How long does it take for IM acepromazine to start acting

A

20-30minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

T/F Medetomidine and dexmedetomidine are more specific for the α2 (vs. α1) receptor than xylazine but also have a longer duration of action

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Why administration of an anticholinergic drug either in combination with the α2-agonist sedative or as a treatment for bradycardia is not recommended

A

Because it provides only a minimal increase in cardiac output and leads to an increased myocardial workload and increased incidence of cardiac arrhythmias.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Why ketamine administration should be carefully considered in a patient with hypertrophic cardiomyopathy?

A

Due to the potential for increased myocardial contractility and oxygen consumption. Ketamine can cause increases in HR, BP and CO, and is associated with endogenous catecholamine release which can predispose to arrhythmias.

In debilitated patients ketamine can cause myocardial depression and hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which of these effects is not expected with ketamine administration?

A.Tachycardia

b. Bronchodilation
c. Severe repiratory depression
d. Increased ICP
e. Increased IOP

A

Although ketamine causes dose-dependent respiratory depression, this is usually transient and ketamine may be useful in patients in which maintenance of spontaneous ventilation is desirable. Ketamine also has bronchodilator activity and may be considered for use in patients with asthma or other causes of bronchoconstriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Ketamine is metabolized by the liver in most species other than ___________, in which it is eliminated unchanged by the kidneys.

A

cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

List examples of sedation protocols that can be useful in patients with upper airway obstruction.

A

Acepromazine 0.005-0.01mg/kg IM
Ketamine (2-4mg/kg) + Diazepam
Propofol low dose with Midazolam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What’s the duration of action of propofol

A

5-10min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Which induction agent can be indicated in a patient with head trauma?

A

Thiopental and propofol do decrease intracranial and intraocular pressure and would be indicated for induction in a patient with head trauma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is propofol28

A

Has a preservative (benzyl alcohol), can be used up to 28 days after first use of the vial and does not need refrigeration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What can be a side effect of propofol28 in cats

A

The benzyl alcohol can be toxic in large doses –> Cats have a low capacity for glucuronic acid conjugation and therefore have limited ability to metabolize benzoic acid

*It may be prudent to avoid the use of PropoFlo 28 in cats that are debilitated or have liver impairment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

MOA of alfaxalone

A

Alfaxalone is a neuroactive steroid molecule with properties of a general anesthetic. The primary mechanism for the anesthetic action of alfaxalone is the modulation of neuronal cell membrane chloride ion transport, which is induced by binding alfaxalone to gamma-aminobutyric acid (GABA) cell surface receptors. Alfaxalone has no analgesic properties.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

The use of etomidate for anesthesia induction in critically ill patients is appealing due to its minimal_________ effects. Etomidate should not be used as the sole induction agent because it may lead to ______________. These adverse effects are minimized by giving a benzodiazepine or opioid IV before etomidate is administered.

A

cardiovascular

retching and myoclonus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Repeated use of etomidate in cats may lead to

A

Hemolysis due to the propylene glycol vehicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

The use of etomidate in critically ill human patients is controversial due to

A

Its ability to cause adrenal dysfunction, which may lead to an increase in morbidity and mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

There are two types of nondepolarizing NMB: aminosteroidal and benzylisoquinolinium compounds. Atracurium, cisatracurium, doxacurium, and mivacurium belong to ___________________

A

benzylisoquinolinium compounds.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

_________is unusual in that its degradation process is independent of enzymatic function; it is inactivated in the plasma by ester hydrolysis and Hofmann elimination, with spontaneous degradation occurring at body temperature and pH

A

Atracurium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

List side effects of the use of atricurium

A
Histamine release (usually not seen at clinical doses)
CNS excitation/seizures and/or hypotension secondary to laudanosine (breakdown product of Hofmann elimination)
Long term neuromuscular weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Monitoring of NMB effects using ________________ is recommended

A

a peripheral nerve stimulator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How can you reverse NMB agents

A

An acetylcholinesterase inhibitor, edrophonium or neostigmine, is used for reversal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

MOA of naloxone

A

Opioid antagonists (e.g., naloxone) bind to the same receptor as agonists but cause no effect and can competitively displace the agonist from the receptor and therefore reverse the agonist effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

The elimination of this opioid is independent of hepatic or renal function because the drug is metabolized by nonspecific esterases in blood and tissues, which makes it an attractive agent for use in patients with hepatic or renal compromise.

A

Remifentanyl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How alpha-2 agonists provide analgesia?

A

The α2 -receptors are abundant in the body and located in the dorsal horn of the spinal cord, brain and periphery. They play an important rol in modulating the pain signals desending from the brain, thereby reducing hyperalgesia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

T/F The sedative effects of medetomidine have a longer duration of action than do the analgesic effects

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Intramuscular or subcutaneous administration of Atipamezole is preferred for reversal because

A

Intravenous administration can lead to abrupt hypotension and/or aggression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How does ketamine provide analgesia

A

Non-competitive NMDA receptor antagonist –> blocks multiple sites at that receptor resulting in analgesic, amnestic and psychomimetic effects, as well as neuroprotection.

Can reverse central hypersensitivity by preventing the exaggerated response, wind-up activity, and central sensitization of wide-dynamic-range neurons in the dorsal horn of the spinal cord.

Ketamine prevents the response to nociceptive stimuli carried by afferent pain neurons (e.g., C fibers).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

T/F In cases of pancreatitis or abdominal pain, bupivacaine (2 mg/kg diluted in saline q6h intraperitoneally) can be administered via an aseptically placed, temporary butterfly catheter to provide analgesia.

A

TRUE - However, However, it may be ineffective when ascites is present due to dilution of the topical analgesic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

In patients undergoing pericardectomy, intrapleural bupivacaine should be used judiciously due to

A

The potential risk of cardiotoxicity –> bupivacaine is selectively cardiotoxic, only half the canine dose should be administered to cats
Intrapleural bupivacaine may also interfere with ventilation by inducing diaphragmatic paralysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Depending on the dose or volume of drug used for epidurals, analgesia of the forelimbs can also be achieved: an injected volume of ____________ blocks to the __________vertebra, and use of a larger volume results in a cranial spread of the analgesia

A

1ml/5 kg

first lumbar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Why is lidocaine helpful in patients with ischemia-reperfusion injury?

A

Lidocaine may help diminish the level of reperfusion injury by inhibiting Na+/Ca2+ exchange and Ca2+ accumulation during ischemia, scavenging hydroxyl radicals, decreasing the release of superoxide from granulocytes, and decreasing polymorphonuclear leukocyte activation, migration into ischemic tissues, and subsequent endothelial dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

List conditions where ketamine could be contraindicated

A

Cardiac disease and hypertension (ketamine has a dose-related sympathomimetic effect)

TBI (ketamine increases cerebral metabolic rate)

Glaucoma/ocular trauma (increases IOP)

Urinary obstruction/urinary bladder rupture in ctas –> can cause prolong effect in cats (they excrete ketamine unchanged in urine).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Why pregnant animals are at increased risk of regurgitation?

A

Progesterone-induced decreased lower esophageal sphincter tone and delayed gastric emptying.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What would be your induction protocol for a patient with GDV?

A

Ketamine + benzodiazepine –> recommended in patients without significant arrhythmias or cardiovascular disease.

Fentanyl, Midazolam, Ketamine for depressed or recumbent patients.

Propofol is less ideal due to the potentialof significant hypotension following administration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is an ideal induction protocol in patient with major wounds?

A

Ketamine + benzo –> ketamine provides analgesia to the skin and muscular tissue.

Propofol, alfaxolone –> are good options, just neither provides additional analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Which one is not an effect/property of acepromazine

a. sedation
b. Anthyarrhythmic
c. Analgesic
d. antihistaminic
e. antiemetic
f. vasodilation

A

c - analgesic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

T/F buprenorphine has a greater potency than morphine but is unable to effect the same maximal level of analgesia

A

TRUE - Potency simply reflects a comparable mg dose and does not reflect the maximal response that an opioid can induce (efficacy). buprenorphine has a greater potency than morphine but is unable to effect the same maximal level of analgesia (less efficacy).

Potency is a description of the amount of drug required to produce an effect. The potency of opioids is ranked by comparison to morphine. Morphine is given a relative potency of 1 and all other opioids are classi- fied based on the equivalent dose required to create the same analgesia as that due to a specific dose of morphine
The efficacy of opioids is the maximal pharmacological effect that the drug can induce. It is unrelated to potency. It is determined by the intrinsic activity of a drug at its receptor. The efficacy of full agonists is greater than that due to partial agonists or agonist/antagonists.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Where are opioid receptors located and how do they act?

A

kappa –> mostly spinal cord and peripheral tissues
Mu –> primarily in CNS but also in peripheral tissues
delta –> associated with the mu receptor

They are part of the G-protein-coupled family –> affect ion channels in pre- and postsyn- aptic nerves. Binding of an agonist to opioid receptors causes a decrease in intracellular cAMP, which results in an increase in potassium movement out of cells and a reduction in calcium movement into cells. Neurons become hyperpolarized, leading to postsynaptic neu- ronal inhibition and a decrease in transmission of infor- mation to the cerebral cortex. It also inhibits presynaptic neurotransmitter release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Which properties make fentanyl a short duration of action agent?

A

Fentanyl is very lipophilic and has a high volume of distribution so it diffuses quickly away from receptors, thus shortening its duration of action.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Opioids - action and receptor

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Why respiratory depression secondary to opioid administration can be problematic in a patient with head trauma or a brain tumor?

A

Opioids depress the respiratory center’s responsiveness to CO2, Respiratory depression can be potentially fatal in patients with pre-existing elevations in intracranial pressure (ICP) such as is associ- ated with head trauma or brain tumors, since the rise in PaCO2 will further increases ICP, potentially leading to brain herniation, coma, and death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Opioids suppress this reflex by stimulation of opioid receptors on A delta fibers that are located in or beneath the respiratory epithelium, independent of their action on the respiratory center.

A

Cough reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

If your patient shows worsening of pain in response to increasing doses of opioids you would suspect _________________. How can you treat this condition?

A

Opioid-induced hyperalgesia

Reduce the dose, alternate opioids
use Methadone that has also antagonist NMDA effects
Use alpha agonists or ketamine or amantadine or lidocaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

T/F opioids inhibit the sacral parasympathetic outflow, especially after epidural administration and after large IV doses, resulting in an increased maximal bladder capacity and detrusor muscle relaxation.

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Explain why some opioids cause vomiting more frequently than others, specially when the first dose is given?

A

Full-agonist opioids both stimulate the chemoreceptor trigger zone (CRTZ), which causes vomiting, and depress the vomiting center which blocks input from the CRTZ. Opioids quickly reach the CRTZ but their lipid solubility determines how fast they cross the blood–brain barrier (BBB) to reach the vomiting center

  • example: Vomiting occurs more frequently with morphine sulfate administration and less commonly with oxymorphone and fentanyl administration. This is because morphine is more water soluble than oxymorphone so crosses the BBB more slowly, allowing time for CRTZ activation to stimulate the vomiting center.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the effect of opioids in the immune system?

A

Immunosuppression –> Opioids have immunomodulatory effects in vitro and in animal models, which are generally believed to increase the risk of infection. However, the clinical significance of opioid-induced immune suppression remains controversial, even in the critical care setting. Like other opioid-induced actions, the immune effects are reversible with administration of an opioid receptor antagonist.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

List at least two contraindications to administer a full mu-agonist

A

Patient with an obstructed oral cavity or evidence of elevated ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Greyhounds may have prolonged recoveries after receiving some anesthetics such as ___________ and may experience ______________ (electrolyte imbalance) associated with general anesthesia.

A

barbiturates

hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Describe a rebreathing anesthesia system, list advantages and disadvantages

A

Anesthesia the flow of gas through the machine is circular: reservoir bag–inhalation valve–inspiration hose–animal–expiration hose–exhalation valve–carbon dioxide canister–back to the inhalation valve. A rebreathing circuit is used for patients weighing over 10 pounds.

Advantages:
Economical: expired oxygen and anesthetic vapor are re-circulated and reused, using less oxygen and anesthetic agent compared with a non-rebreathing system.
Humidification of inspired gas, preserving heat and moisture of the patient.
Warmth: during the absorption of CO2 in soda lime, heat is generated. This helps to preserve further body heat.

Disadvantages
Resistance to gas flow, primarily caused by one way valves in the system, soda lime canister, and pressure relief valve.
Can make it difficult for small patients to ventilate
A minor disadvantage of lower flow rates is increased time to change anesthetic depth after changing the vaporizer setting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Describe a non-rebreathing anesthesia system, list advantages and disadvantages

A

In this circuit, oxygen flows through a flow meter and into the vaporizer. At this point, gases exiting the vaporizer go directly to a hose for delivery to the patient with no inhalation flutter valve. Exhaled gases pass through another hose and may enter a reservoir bag, but do not enter a CO2 absorber. The gas is then released into a scavenger. Used for patients weighing less than 10 pounds.

Advantages:
Less resistance to breathing.
Less mechanical dead space.
Rapid manipulation of anesthetic depth: in NRB the fresh gas inlet is adjacent to the endotra-cheal tube connection; changes in flow meter or vaporizer settings affect the inspired gas concentration almost immediately. (Volume of rebreathing circuit with a 3L bag is approxi-mately 6L. Volume acts as a “buffer” to changes in anesthetic concentration.)

Disadvantages
High flow of dry cool gas is administered to the patient, which can cause significant heat and humidity loss.
This can contribute to hypothermia, especially in small patients.
Significantly higher waste of both carrier gas and anesthetic agent results in increased costs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Two essential safety features to have on every anesthetic machine are

A

(1) an in-circuit manometer

(2) a safety pop-off valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

For a small patient which would be better:
Non Rebreathing circuit (NRC)
Rebreathing circuit (RC)

A

NRCs are commonly used for cats and small dogs (patients ,3–5 kg [6.6–11 lbs]) because, compared with RCs, they cause less resistance to breathing and have low equipment dead space, both of which are important considerations in small patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

During anesthesia, dead space should be kept to a minimum and should be _________, which is _____% of total tidal volume

A

<2–3 mL/kg

<20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Rebreathing of CO2 in the NRC is prevented by _________, which also allows for a faster turnover in the change of anesthetic depth when adjusting the vaporizer setting.

A

High O2 flow rates

Thus, the O2 flow should be w200–400 mL/kg/min when using NRCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

the oxygen flush valve should never be used in a patient breathing through an ________ because it directs a high-pressure flow directly into the patient’s airway, potentiating barotrauma.

A

NRC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Give an example of each:
Passive scavenge system
Active scavenge system

A

Passive scavenge system: charcoal canister

Active scavenge system: succion of vacuum system, ventilation system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

How do you choose the size of the reservoir bag in the anesthesia circuit?

A

Tidal volume (10-20mL/kg) x 6

89
Q

The oxygen flush valve should never be used in a patient breathing through an ________________because it directs a high-pressure flow directly into the patient’s airway, potentiating barotrauma.

A

Non-rebreathing system

With the non-rebreathing system if you want to do the leak test, only turn on the oxygen to fill the system.

90
Q

In a rebreathing circuit –> During the maintenance phase, total O2 flow rate should typically be ______mL/kg/min, with a minimum ___mL/min to ensure accurate vaporizer output.

A

20–40 ml/kg/min

500 ml/min

91
Q

Based on a recent study conducted in a veterinary ICU, what was the overall prevalence of pain in hospitalized dogs? In which services where most likely to be characterized as painful?

A

22%

Orthopedic and neurosurgery

92
Q

T/F - Pain can increase subcutaneous oxygen tension and helps wound healing

A

FALSE - pain DECREASES subcutaneous oxygen tension and may impair wound healing

93
Q

What is central sensitization?

A

When nociceptor stimulation persists unmitigated and leads to increase responsiveness of dorsal horn neurons -> wind up or hyperalgesia.

This can decrease the efficacy of analgesic drugs and require higher doses, resulting in more pronounced side-effects.

94
Q

Summarize conclusions of Muir’s study of pain in the emergency department

A
  • Painful dogs were significantly older and heavier
  • The majority had acute pain of mild-to-moderate severity, somatic in origin (skin and ortho predominant).
  • Painful cats -> also older, pain was more chronic and visceral in origin -> pancreatitis, colitis or obstruction (urethral / constipation) the most common.
95
Q

Which are the most common effects of opioids in small animals? Are those different than in humans?

A
  • Few cardiovascular effects - vaguely mediated bradycardia, more common with the more potent opioids (fentanyl, remifentanyl).
  • Respiratory depression is a major side-effect in humans -> in vet med is more common GI ileum and dysphoria.
96
Q

Why the use of meperidine and / or morphine can decrease vasomotor tone?

A

They are associated with histamine release.

97
Q

Which opioids have the most sedative effects?

A

Morphine and butorphanol.

98
Q

What is neuroleptanalgesia

A

Use the combination of a tranquilizer with an analgesic, using their synergistic effects.

99
Q

Opioid reversal

A

Naloxone

100
Q

Benzodiazepines reversal

A

Flumazenil

101
Q

Why alpha-2 agonist can cause a decreased CO?

A

They cause initial peripheral vasoconstriction and reflex bradycardia.

102
Q

Why are alpha-2 agonists relatively contraindicated in patients with urinary obstruction?

A

They increase urine output.

103
Q

Why phenothiazines should be avoided in patients that are cardiovascular unstable?

A

They are irreversible smooth muscle vasodilators (via alpha-1 antagonism) and can result in hypotension.

104
Q

How do NMDA antagonists modulate pain?

A

They modulate pain at the level of the spinal cord, reducing central sensitization.

Analgesia and sedative effects are best when combined with an opiod and/or benzodiazepines.

105
Q

In which patients should ketamine be avoided?

A
  • Ketamine has a dose-dependent sympathomimetic activity -> caution in patients with cardiac disease or hypertension.
  • Increases cerebral metabolic rate -> not recommended in patients who are or may be at risk of increased ICP (TBI).
  • Causes mild increase in IOP -> caution in ocular trauma or glaucoma.
  • Excreted unchanged in urine -> if we use it for a urinary blockage -> sedation may persist until urine evacuated.
106
Q

Do most induction drugs provide analgesia?

A

No

107
Q

When is respiratory depression and vasodilation more potent with propofol, when administered as a bolus or as a CRI?

A

As a bolus

108
Q

Dose of propofol CRI to maintain sedation

A

50-100 ucg/kg/min

109
Q

What can repeated doses of propofol cause in cats?

A

Heinz body anemia - avoid prolonged use

110
Q

Why induction with inhaled agents is not recommended?

A
  • High doses required -> can result in significant hypotension and hypoventilation.
  • Slower induction process -> can cause emesis when patient is unable to protect airway.
  • If using a container -> when opening it a lot of gas will come out -> personnel!
  • If using a mask -> stressful for the animal.
111
Q

Main anesthetic concerns for the dam before/during a c-section

A
  • Might have been in labor for a prolonged period of time: hypoglycemia and/or hypocalcemia -> might require supplementation prior to anesthesia.
  • Pregnant animals -> increased risk of regurgitation and aspiration due to a progesterone-induced decrease in LES tone and prolonged gastric emptying.
  • High levels of progesterone -> 16% to 40% decrease in minimum alveolar concentration of inhalant anesthetics.
  • Uterus reduces dam’s functional residual capacity and oxygen reserve + increased oxygen consumption due to pregnancy -> hypoxia even in short periods of apnea.
  • Ventilation and venous return can be impeded when the dog is in dorsal recumbency.
112
Q

Main anesthetic concerns for the neonates before/during a c-section

A
  • All anesthetic drugs cross the placenta barrier -> neonatal depression.
  • Fetal blood flow is dependent on maternal CO -> anything that decreases uterine arterial flow will decrease fetal oxygen and nutrient delivery.
  • Respiratory depression very concerning in neonates -> small changes in tidal volume and RR can result in hypoxemia.
113
Q

Which drug should be avoided for a c-section as it has been associated with decreased fetal survival?

A

Xylazine

114
Q

Why are propofol / alfaxalone good induction agents for c-section

A

Short half-life and rapid metabolism

115
Q

What type of regional block can be done in a c-section?

A

Incisional line block with lidocaine / bupivacaine

116
Q

Maintenance anesthesia for c-section?

A
  • Avoid excessive inhalant agents to minimize neonatal apnea.
  • They will be rapidly cleared as long as the neonate is breathing.
117
Q

Pain relief for dam during c-section

A
  • Buprenorphine IV/IM - long duration and minimal cardiovascular and respiratory effects.
  • Single dose of carprofen -> as long as MAP >60mmHg during surgery and preoperative bloodwork ok.
118
Q

Anesthetic concerns for enucleation

A
  • Oculocardiac reflex -> mediated by the trigeminal and vagus nerve, can result in dysrhythmias like bradycardia, VPCs or asystole.
  • Drugs that cause vomiting -> vomiting will increase IOP.
  • Transient increase in IOP during intubation due to stimulation of larynx / pharynx.
  • Enucleation is painful, proper analgesia is needed.
119
Q

Why should we consider to administer an anticholinergic in the premedication for a patient with an ocular trauma?

A

To reduce the risk of oculocardiac reflex during surgery.

120
Q

Enucleation premedication

A

Opioid + benzodiazepines / phenothiazine

+/- anticholinergic (atropine / glycopyrrolate)

121
Q

What is the main electrolyte we might need to correct before surgery for a GI FB?

A

Hypokalemia - can cause muscle weakness, GI ileus and arrhythmias

Supplement as a CRI, max 0.5mEq/kg/h

122
Q

If we are trying to scope out a FB, which drugs could potentially increase the pyloric sphincter tone, making it more difficult to pass the scope to the duodenum?

A

Opioids and atropine.

123
Q

What can happen with overinsufflation of the stomach during endoscopy?

A
  • Decreased venous return

- Vasovagal stimulation -> bradycardia.

124
Q

Why ketamine + benzodiazepines is a good combination for induction agent in x-laps?

A
  • Good especially in hemodynamically compromised patients -> ketamine acts as sympathomimetic, providing cardiovascular support as well as somatic analgesia.
  • if hemodynamically stable, propofol / alfaxalone are suitable alternatives - do not provide analgesia.
125
Q

Anesthetic concerns in GDV

A
  • Significant impairment of venous return to the heart.
  • Gastric dissension prevents caudal displacement of diaphragm -> decreased lung complicance and functional residual capacity.
  • Arrhythmias are common -> tachycardia, V-tach, VPCs.
  • Splenomegaly can occur secondary to displacement by rotated stomach.
  • Hemoabdomen can happen if rupture of short gastric vessels
  • Painful condition - analgesia as part of the initial therapy.
126
Q

Full mu agonists are the drug of choice of GDV / GI FB due to…

A

Their MAC-sparing effects and minimal cardiovascular effects.

127
Q

GDV and induction agents

A
  • Ketamine + benzodiazepines - in patients w/o significant arrhythmias or cardiovascular disease.
  • Propofol less ideal due to hypotension following IV administration.
  • Recumbent patients: fentanyl + midazolam + ketamine
128
Q

Inhalant gases and GDV/ GI FB

A
  • Nitrous oxide contraindicated -> will diffuse rapidly into gas-filled compartments, increasing intragastric volume and organ distension.
129
Q

Resuscitation goals for hemoabdomen patients prior to sx

A
  • HR < 150bpm
  • SBP > 90mmHg
  • PCV / TP - no lower than 20% and 4g/dL ->If PCV <20%, or blood loss is >20% of the blood volume of the patient, consider whole blood / pRBCs transfusion.
  • Decreasing lactate
130
Q

Anesthetic concerns for hemoabdomen

A
  • Continued blood loss until source of bleeding is controlled.
  • Hypovolemia -> with anesthetic agents can lead to profound hypotension.
  • Cardiac arrhythmias are common.
131
Q

Why is ketamine a good induction agent for wound repairs?

A

It provides analgesia to the skin and muscular tissue.

132
Q

Anesthetic concerns in patients with AV block that undergo pacemaker placement?

A
  • They already have reduced CO -> increased risk of hypotension.
  • Introducing catheter and pacemaker in the heart might induce arrhythmias.
133
Q

Premedication and induction for pacemaker

A
  • Full mu-agonist + benzodiazepine.
  • Induction -> if heart disease, etomidate. If not, propofol / alfaxalone are ok.
  • DO NOT CONFUSE scape beats with arrhythmias -> suppression can result in cardiac arrest!
134
Q

Canine urethral obstruction - preanesthetic considerations

A
  • Hyperkalemia can result in bradyarrhythmias and cardiac arrest -> stabilize before anesthesia (calcium gluconate, dextrose +/- insulin, bicarbonate, B-2 agonists).
  • Hyperkalemia can be exacerbated with hypoventilation and respiratory acidosis -> intermittent PPV to maintain normocapnia (PaCO2 35-45mmHg)
135
Q

Why is intubation recommended in brachycephalic dogs, even for short and non painful procedures?

A

Because they are at risk of upper airway obstruction, regurgitation and aspiration pneumonia.

136
Q

Which opioids cause more hyperthermia and dysphoria in cats, full mu-opioids or partial mu-opioid agonists?

A

Partial - buprenorphine

137
Q

Side effects of full mu-agonist agents in dogs

A
  • Centrally mediated, vaguely induced bradycardia (methadone > others like morphine)
  • Panting, dysphoria
  • Ileus, vomiting
  • Sedation, hypothermia
  • Miosis, respiratory depression - reduced response to CO2
  • Defecation
138
Q

Side effects of full mu-agonist agents in cats

A
  • Similar like dogs, but sometimes CNS excitation instead of sedation occurs.
  • Mydriasis
  • Hyperthermia
  • Less often, defecation.
139
Q

Why is methadone different from all other mu-agonists?

A

It has NMDA antagonist properties -> may be useful in patients experiencing hyperalgesia or chronic pain.

140
Q

Dose of butorphanol to be used as a reversal for opioids

A

0.05mg/kg IV to effect.

141
Q

In which patients should we avoid the use of alpha-2 agonists?

A

Patients with

  • Degenerative valvular disease
  • Systolic dysfunction
  • Reduced CO and oxygen delivery
  • Critically ill patients
  • Bradyarrhythmias like SSS or 3rd degree AV block
142
Q

In which situation has dexmedetomidine show to be of benefit in cats?

A

In those with LV outflow tract obstruction

143
Q

Other properties of ace other than sedation

A

Antiemetic.

Antiarrhythmic.

Anithistaminic.

Can be used in patients with seizures as it does not affect the seizure threshold.

Useful in patients where an increase in after load is not desired (degenerative valve dx or pulmonic stenosis)

144
Q

In which patients is safe to use benzodiazepines?

A

Patients with cardiac, respiratory, renal or neurological diseases.

They cause minimal cardiorespiratory depression, maintain CO and renal perfusion and suppress seizure activity.

145
Q

In which patients is controversial the use of benzodiazepines?

A

In patients with hepatic disease due to their dependence of phase I hepatic metabolism.

146
Q

Propofol side effects

A
  • Dose dependent.

- Vasodilation, respiratory depression and reduced CO.

147
Q

T/F Alfaxalone has a similar pharmacodynamic profile to propofol in dogs and cats, although it may cause less vasodilation and less reduction in CO

A

TRUE.

148
Q

When is particularly helpful alfaxalone?

A

In sedating aggressive animals in the ER whose underlying cardiac status is unknown.

149
Q

Why is ketamine becoming more commonly used as part of procedural sedation in pediatric emergency rooms?

A

Rapid effects.
Lack of cardiorespiratory depression.
Provides analgesia.

150
Q

Ketamine side-effects

A

Myoclonus, dysphoria, increased ICP, possible pain on injection.

151
Q

What is ketofol

A

Propofol + ketamine (same syringe) - used as rapid induction agent with analgesic properties.

152
Q

Name adverse drug-drug interactions

A
  • Combinations of sedative analgesics -> promote excessive CNS depression or inability to protect airways
  • Drugs which increase the risk of serotonin syndrome -> ss resulting from routine doses of anxiolytics and opioids is not generally an issue in vetted, but caution is advisable.
  • Potentiation of inhalant or IV anesthetics by analgesics -> when opioids, local anesthetics, ketamine or alpha-2 ago snits are used, requirements for inhaled anesthetics are less, needs to be taken into account.
  • Use of 2 drugs in succession with similar toxicities -> switching from a non-selective o a COX2 selective NSAID is thought to pose a significant GI ulceration risk.
153
Q

Why are loading doses of NSAIDs not recommended?

A
  • Potential for toxicity
  • Accidental failure to reduce to maintenance dosing
  • Humans -> increasing the dose of NSAID tends to increase duration rather than magnitude of effect.
154
Q

How is expected pain to progress?

A
  • To increase as the post injury inflammatory response proceeds.
  • Most humans report that pain after strenuous activity becomes evident within 12-24h.
155
Q

If pain is of greater magnitude or duration than expected despite treatment, what should we suspect?

A

Complications -> wound infection, dehiscence, nerve impingement, fracture, ischemia, bandage/splint pain, gastric / esophageal ulceration, urinary retention, delayed gastric emptying and pancreatitis.

156
Q

Opioids side-effects

A
  • Nausea, vomiting, inappetence, ileus, urinary retention -> with mu-agonists-
  • Respiratory depression is of concern with moderate-to-severe pulmonary dysfunction, increased ICP and acidosis.
  • Opioids are potent cough suppressants -> in patients with airway compromise or V/R, it may lead to significant morbidity.
  • Dogs receiving mu-agonist opioids have altered thermoregulatory set points -> leads to a mild hypothermia (98F)
157
Q

T/F - SQ administration of opioids is not recommended as it produces erratic and poor analgesia

A

TRUE

158
Q

If buprenorphine is used to treat pain, should it be withhold to be able to switch to a full mu-agonist?

A

No, as that will lead to a gap in analgesia.

There will be unbound mu-receptors available, therefore it is not a major limitation to continue buprenorphine until the time that the full mu-agonist is given.

159
Q

When is prostaglandin inhibition (with NSAIDs) contraindicated?

A
  • Volume depletion
  • Poor CO
  • Pre-existing renal compromise -> kidneys rely on PG to improve renal blood flow.
160
Q

Washout period between administration of different NSAIDs

A

5-7 days

Aspirin > 7 days

161
Q

T/F - local anesthetics are very effective for acute pain; beyond analgesia, they also have broad anti-inflammatory and antimicrobial effects

A

TRUE

162
Q

T/F - intravenous lidocaine should be used with caution and possibly lower doses in dogs with hypoalbuminemia or poor cardiac output due to increased risk of toxicity

A

TRUE

163
Q

Is intravenous lidocaine recommended in cats?

A

No, because of poor ability to metabolize the drug.

164
Q

Benefits of “low-dose” or “micro-dose” ketamine

A
  • 0.6mg/kg/h
  • Demonstrated to improve opioid sparing, prevent opioid tolerance and reduce acute somatic and visceral pain.
  • Also potential to reduce production of proinflammatory cytokines
165
Q

T/F dexmedetomidine produces sedation and at higher doses (>5mcg/kg/h), analgesia

A

TRUE

166
Q

T/F - Dexmedetomidine reduces cardiac index

A

TRUE

167
Q

T/F - At higher or low doses of dexmedetomidine, CI is reduced by ______

A

30-50%

168
Q

Gabapentin in critically ill

A
  • Relatively non-toxic even at high doses
  • Consider dose reduction in hepatic / renal dysfunction
  • Can be combined with other analgesics
  • Mixed results in different studies regarding its efficacy in reducing postoperative pain.
169
Q

T/F - Cryotherapy (ice packs, crushed ice…) is typically used after recent injury or during active inflammation and is easily applicable in dogs, not that easy in cats.

A

TRUE

170
Q

How are opioids classified?

A
  • Based on the specific receptor(s) they bind to
  • Their affinity for the receptor(s)
  • The action at the receptor(s)
  • Also based on their potency and efficacy.
    • Potency - amount of drug required to produce an effect - always ranked comparing to morphine (given a relative potency of 1).
    • Efficacy - maximal pharmacological effect that a drug can induce - unrelated to potency. It is determined by the intrinsic activity of a drug at its receptor -> efficacy of full-agonists > partial agonists or agonist/antagonist.
171
Q

Opioid categories

A
  • Full agonist -> when bound to its receptor, activates it to its maximal response
  • Partial agonist -> when bound to its receptor, activates it to a level below the maximal response. Increasing the dose of a partial agonist over the maximal therapeutic dose does not result in greater analgesia or more severe side effects.
  • Agonist/antagonist -> a drug that acts simultaneously on different receptor subtypes, functioning as an agonist at one or more receptor subtype and as antagonist at another one or more subtypes. They have also a ceiling effect like partial agonists - will not induce extreme respiratory depression or bradycardia with increasing doses. Due to the antagonist effects they are useful at reversing the effects of full-agonist opioids while they still provide some analgesia.
  • Antagonist -> when bound to its receptor does not produce any stimulation.
172
Q

Where are the opioid receptors localized?

A
  • Brain and spinal cord
  • Brain -> highest concentration in the thalamus.
  • Spinal cord -> substantia gelatinosa - on synaptic membranes where they regulate the transmission of information from primary sensory pain afferents. They also block the release of substance P - important NT of painful stimuli, in the dorsal horn of the spinal cord.
173
Q

Opioid receptors and locations

A
  • Kappa -> spinal cord and peripheral tissues
  • Mu -> CNS mainly but also in peripheral tissues
  • Delta -> associated with mu receptors.
  • G-protein-coupled (Gi) -> an agonist will cause a decrease in cAMP -> increases K efflux and decreases Ca influx -> hyper polarization and postsynaptic neuronal inhibition. Also inhibits presynaptic NT release.
174
Q

Opioids action and receptors

A
175
Q

Does epidural administration of opioids cause motor paralysis?

A

No

176
Q

Dose and location of opioid epidural administration

A
  • Lumbosacral junction

- Preservative free morphine - 0.1-0.2mg/kg (1/10th of the parenteral dose)

177
Q

Why normally PO, OTM, SQ and IM routes are not very much used in critically ill patients?

A

Because this patient population often present challenges in predicting uptake from GI and peripheral tissue due to underlying diseases.

178
Q

What does the administration of oral buprenorphine requires in order to have a good bioavailability?

A
  • Normal oral pH

- Significant dental disease can lower oral pH and reduce bioavailability

179
Q

Duration of fentanyl patches in dogs and cats

A
  • Dogs - 3 days

- Cats - 4 days

180
Q

T/F - Buprenorphine is easy to titrate to effect, like the rest of the opioids

A

FALSE -> difficult to titrate due to the relatively long time (15-30min) it takes to reach peak effect after IV administration, and its high affinity for the mu-receptor, which makes it very difficult to reverse.

181
Q

Advantages and side-effects of opioids (general categories)

A
Respiratory effects
Antitussive
Effects on body temperature
Opioid-induced hyperalgesia
Urine retention
Dysphoria
Bradycardia
Vomiting/nausea/defecation
Histamine release
Immunosuppresssion
182
Q

Respiratory effects of opioids

A
  • Decrease the respiratory center’s responsiveness to CO2
  • Dose dependent increase in PaCO2 -> decreased minute ventilation (low RR, but TV might also decrease).
  • Can be potentially fatal in patients with increased ICP (head trauma, brain tumors), as raises in PaCO2 will further increase ICP -> lead to brain herniation, coma, death.
  • Increases in PaCO2 will worsen acidosis
    • In hyperkalemic patients due to renal disease, worsening acidosis further increases blood K levels.
183
Q

Opioids antitussive effects

A
  • Mediated by opioid receptors on A delta fibers, that are located in or beneath the respiratory epithelium.
  • Independent of their action on the respiratory center.
  • Should be avoided in patients with risk of regurgitation and aspiration pneumonia, especially brachycephalic with pre-existing evidence of dyspnea / asp. pneumonia.
  • Also in post op tieback sx -> higher risk of AP.
184
Q

Opioid-induced hyperalgesia

A
  • Worsening pain in response to increasing doses of opioids.
  • Reduce dose of opioid or rotate opioid use.
  • Methadone -> NMDA antagonist - multimodal effect.
  • Ketamine, amantadine, dexmedetomidine CRI or lidocaine CRI will reduce the dose of opioid needed.
185
Q

Opioids and urine retention

A
  • Occurs with mu-agonists
  • Dose related
  • Fentanyl > buprenorphine… lesser extent, morphine.
  • Opioids inhibit the sacral parasympathetic outflow, especially after epidural and large IV doses -> increased maximal bladder capacity and detrusor muscle relaxation.
186
Q

Opioids and bradycardia

A
  • Central stimulation of vagal input can result in bradycardia.
  • Effect more severe in hypothermic patients.
187
Q

Opioids and V / nausea / defecation

A
  • Usually occurs only with the first dose.
  • Full-agonists stimulate the CRTZ, which causes vomiting, and depress the V center which blocks input from the CRTZ.
  • Opioids quickly reach the CRTZ but their lipid solubility determines how fast they cross the BBB to reach the vomiting center.
188
Q

Why morphine and meperidine should not be administered IV?

A

They induce histamine release - if needed, administer IV slow (2-3min) and monitor for signs of hypotension, shock or cutaneous signs.

189
Q

Immunosuppression and opioids

A
  • They have immunomodulatory effects in vitro.

- Clinical significance unknown.

190
Q

T/F - sedation, anxiolytics and analgesia provided by alpha-2 agonists is dose independent

A

FALSE - it is dose dependent.

191
Q

Alpha 2 receptor subtypes

A
  • Alpha 2A - primary located in CNS (cerebral cortex and locus ceruleus) -> supraspinal analgesia, sympatholytic effects and sedation.
  • Alpha 2B -> spinal cord and vascular endothelium -> initial vasoconstriction and allows for spinal analgesia.
  • Alpha 2C -> responsible for mediating hypothermia.

All of them GPCR

192
Q

Alpha-2 agonist drugs

A

Dexmedetomidine
Medetomidine
Xylazine

193
Q

Duration of dexmedetomidine in SA

A

1 - 2 hours

194
Q

Main physiological alterations after alpha2 administration

A
  • Increased SVR
  • Bradycardia
  • Combination of those 2 decreases CO by 30-50%, depending on dosage.
  • Delayed phase (45-60min after initial administration) -> decreased sympathetic output -> continued bradycardia and hypotension.
195
Q

How does dexmedetomidine increases urine output?

A

Interferes with ADH action at the level of the renal tubules and collecting ducts.

196
Q

Dexmedetomidine effects on IOP and pancreas

A
  • Will cause vomiting most of the times - avoid in patients with ocular dz as vomiting will increase IOP.
  • Transient hypoinsulinemia and hyperglycemia due to effect on pancreatic B-cells.
197
Q

T/F Use of dexmedetomidine CRI has proven an equivalent if not superior alternative to bentos in MV human patients, with fewer behavioral alterations and reduced ventilator times.

A

TRUE

198
Q

T/F Alpha2 agonists can be used alongside a local anesthetic to prolong and intensify peripheral nerve blockade.

A

TRUE

199
Q

2 positive benefits of alpha-2 agonists

A
  • Immunomodulatory properties - anti-inflammatory potential, may ultimately improve patient outcome.
  • Reversibility - if patient is not critical, administer IM, as rapid IV atipamezole can cause hypotension.
200
Q

Types of pain

A
201
Q

Allodynia

A

Pain caused by non painful stimulus

202
Q

Definition of nociception

A

Stimulation of sensory nerve cells called nociceptors, which produce a signal that will travel along a chain of nerve fibers via the spinal cord, to the brain.

203
Q

Nociception pathway

A
204
Q

Phases of nociceptive pain

A
205
Q

Transduction phase of nociceptive pain

A
206
Q

Nociceptive pain - transmission

A
207
Q

A -B fibers

A
208
Q

A - delta fibers

A
209
Q

C fibers

A
210
Q

Types of C fibers

A
211
Q

T/F - 1st order neurons from nociceptors goes to the dorsal horn and reed laminae

A

TRUE

212
Q

Rexed laminae

A
213
Q

Limbic system

A
214
Q

Nociceptive pain - modulation

A
215
Q

Endogenous mechanisms of pain modulation

A
216
Q

Descending inhibitory nerve system

A
217
Q

Endogenous opioid system

A
218
Q

Peripheral modulation of nociceptors

A