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ECVECC Board Exam > Anesthesia/Pain Management > Flashcards

Anesthesia/Pain Management Flashcards

1
Q

What is the contraindication for interpleural analgesia?

A

When pericardium is disrupted

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2
Q

How to perform an interpleural analgesia?

A

1) Prepare bupivacaine 1.5 mg/kg
2) 1 to 4 dilution with normal saline
3) Slowly infuse the solution into the chest tube and allow it to sit for 30 minutes. Keep the incision side down
4) Same procedure can be repeated q4-6h, with the max dose of 9mg/kg/d

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3
Q

How many percentage of PCV can decrease during anesthesia?

A

3-5%

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4
Q

Which induction agent can cause adrenal suppression?

A

Etomidate

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5
Q

How is remifentanil metabolized?

A

Non-specific esterases in the blood

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6
Q

How is atracurium metabolized?

A

Partially by ester hydrolysis
Partially by Hofmann elimination (spontaneous degradation in normal temperature & pH)

  • Hofmann elimination is sowed down by acidosis and hypothermia
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7
Q

What are potential side effects for atracurium administration?

A

1) laudanosine release (product from Hoffman elimination) → CNS excitement
2) Histamine release

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8
Q

What is the reversal for neuromuscular blockage?

A

edrophonium, neostigmine (anticholinesterase)

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9
Q

What is the dose, onset and duration of neostigmine?

A

Onset 7-10 min
Duration 60-70 min
Dose 0.04 mg/kg IV

*Can combine with glycopyrrolate 0.01 mg/kg to combat bradycardia

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10
Q

Which electrolytes are GABAA receptor coupled with?

A

Chloride
GABAa receptor is a ligand-gated chloride channel

  • GABAA (fast response) receptors are anion channels whereas the GABAB (slow response) receptors are G‐protein‐coupled receptors
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11
Q

How does GABAa receptor work when it’s activated?

A

It allows chloride to enter the cell → hyperpolarization of the cell → inhibit the cell to subsequent depolarization → CNS depression

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12
Q

What are the agonists for AMDA and NMDA receptor?

A

Glutamate

*Aspartate is also an endogenous agonist for NMDA receptor
* glycine is a co‐agonist required to open the NMDA channel efficiently

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13
Q

How does NMDA receptor work when it’s activated?

A

NMDA receptor It allows Na and Ca to enter the cell & K to leave the cell → cell is more likely to depolarize → excitatory effect

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14
Q

Where are NMDA receptor most commonly found in the neuron.

A

Post-synaptic membrane

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15
Q

True or False: ATP is the main source of energy for G-protein coupled receptor.

A

False

Guanosine triphosphate (GTP) is the energy

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16
Q

Explain how does G-protein coupled receptor work.

A

There are two types of G proteins, Gs (stimulation) and Gi (inhibitory). When the receptor binds to an agonist, both the receptors and G protein change their conformations → the GDP attached on the G protein (𝜶 unit) is replaced by GTP → stimulate/inhibit the adenylyl cyclase or other membrane enzymes → AC uses ATP to produce cAMP → activate/inhibit protein kinase A → downstream enzyme production & cell signaling

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17
Q

Define potency.

A

The concentration of the drug needed to achieve a pharmacological effect equal to 50% of Emax.

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18
Q

Which cholinergic receptors do atropine and glycopyrrolate mainly inhibit? muscarinic or nicotinic?

A

Muscarinic

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19
Q

Which of the anticholinergics can cross BBB? Atropine or glycopyrrolate?

A

Atropine

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20
Q

When you give low dose atropine, why sometimes you will see transient bradycardia and 2nd degree AV block prior to tachycardia?

A

The presynaptic M1 receptors are blocked first, which inhibit the negative feedback inhibitory effect → more acetylcholine release
*usually after a while once the postsynaptic M2 receptors are blocked, bradycardia will resolve.

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21
Q

What are the MOA for 𝜶1 and 𝜶2 adrenergic receptors?

A

𝜶1: excitatory G protein-coupled receptor linked to phospholipase C → increases intracellular inositol triphosphate → increase in intracellular [Ca2+]
𝜶2: inhibitory G protein-cpupled receptor linked to adenyly cyclase → decrease cAMP

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22
Q

True or False: 𝜶2 adrenergic receptor activation can lead to platelet aggregation

A

True

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23
Q

What is the MOA for 𝜷1 and 𝜷2 adrenergic receptors?

A

𝜷1 and 𝜷2: excitatory G protein-coupled receptor linked to adenylyl cyclase → increase cAMP

  • 𝜷2: increased cAMP activates protein kinase A → increase activity of Na/K ATPase → hyperpolarization → smooth muscle relaxation
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24
Q

What are the MOA for dopamine1 and dopamine2 receptors?

A

D1: excitatory G protein-coupled receptor linked to adenylyl cyclase → increase cAMP
D2: inhibitory G protein-cpupled receptor linked to adenyly cyclase → decrease cAMP

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25
Q

How does epinephrine cause hyperglycemia?

A

1) inhibition of insulin secretion (α2‐ and β2‐adrenergic effect)
2) glycogenolysis in liver and muscle (α1‐ and β2‐adrenergic effect)
3) lipolysis (β2‐ and β3‐adrenergic effect)
4) gluconeogenesis (α1‐ and β2‐adrenergic effect)

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26
Q

What are the predominant receptors dopamine work on at different CRI rate?

A

1-2 mcg/kg/min: D1 & D2 receptors
2-10 mcg/kg/min: 𝜷1 adrenergic receptors
> 10 mcg/kg/min: 𝜶1 adrenergic receptors

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27
Q

Is propanolol a 𝜷1 or 𝜷2 antagonist?

A

It is a non-selective 𝜷 receptor antagonost

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28
Q

What is MOA for acepromazine?

A

dopamine receptor antagonist → sedation
𝜶1 adrenergic receptor antagonist → vasodilation
histamine 1 receptor antagnoist

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29
Q

How does 𝜶2 agonist cause bradycardia?

A

Vasoconstriction → baroreceptor-mediated reflexes → bradycardia

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30
Q

What is the MOA for opioid receptor?

A

Gi protein-coupled receptor → inhibition of adenylyl cyclase → decrease cAMP production → inhibition of Ca2+ channels in presynaptic neurons → decreased release of excitatory neurotransmitters (e.g., glutamate and substance P)

decrease cAMP production → enhancement of cellular K+ outflow in postsynaptic neurons → hyperpolarization of nociceptive neurons and nociceptors → increased activation thresholds

  • In supraspinal area, opioid binds to receptors within the periaqueductal gray (PAG) region → release dopamine and glutamate → supraspinal antinociception effect
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31
Q

What are the two neural fibers mediated pain?

A

C fibers: slow‐conducting, unmyelinated nerves associated with dull aching pain
A 𝛅 fibers: fast‐conducting, myelinated nerves associated with sharp, discrete pain

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32
Q

What are the five phases of pain transmission?

A

1) Transduction
2) Conduction
3) Transmission
4) Modulation
5) Perception

33
Q

How does opioid cause respiratory depression?

A

supraspinal μ opioid receptors activation

34
Q

What is the MOA of the emetic effect of opioids?

A

Stimulation of D2 receptors in the CRTZ (𝛅 receptors are involved)

*𝜇 and ĸ receptors have anti-emetic effects

35
Q

What are the two opioids that demonstrate plateau effect?

A

Butorphanol
Buprenorphine

36
Q

What is the proposed MOA for tramadol’s analgesic effect?

A

Tramadol’s metabolite - O-desmethyltramadol acts as a full 𝜇 agonist

  • Dogs do not make enough O-desmethyltramadol
  • Cats make enough
37
Q

Which cholinergic receptor exist at the neuromuscular junction? muscarinic or nicotinic?

A

Nicotinic

38
Q

During normal neuromuscular transmission, acetylcholine binds to junctional receptors and how is the cell activated?

A

Conformation change → Na and Ca enters the cell while K exits the cell

39
Q

For neuromuscular blocking agents, there are depolarizing agent and non-depolarizing agent. What are the MOA for them and name an example for each category of them.

A

Depolarizing agent
- The drug binds to the nicotinic receptors and activates the receptors, but they are not broken down by acetylcholinesterase so the ion channels remain open → inexcitability of the motor endplate
- Succinylcholine

Non-depolarizing agent
- The drug binds to the nicotinic receptors but do not activate them → flaccid paralysis
- Atracurium

40
Q

What is the onset and duration of atracurium?

A

Onset: 5min
Duration: 30 min

41
Q

For the monitoring of atracurium, describe the technique of train of four and what is considered adequate effect?

A

The machine will deliver four supramaximal impulses over 2 s (2 Hz) to the muscles. The level of relaxation will be determined by comparing the intensity of the fourth twitch to the first twitch. Before NMBA is administered, the T4:T1 will be 1.0. After the NMBA is given, the fourth twitch will become weaker/disappear first, followed by the 3rd, 2nd and 1st. During the recover, the T4:T1 ratio > 0.7 is considered adequate recovery from muscle relaxant.

42
Q

What is the dose for atracurium for mechanical ventilation?

A

Loading dose: 0.2-0.5 mg/kg
CRI (5 minutes later): 3-9 mcg/kg/min

Dilute with NS or D5W

43
Q

What are the two possible side effects for acetaminophen?

A

1) Hepatic toxicity
2) Methemoglobinemia

44
Q

Why acetaminophen is contraindicated in cats?

A

Cat is deficient of glucuronyl transferases (enzymes for glucuronidation) so they cannot metabolize acetaminophen well through that pathway. The majority of the Acetaminophen will be metabolized by cytochrome p450 and produce NAPQI, which is a very toxic free radicals.

  • NAPQI usually is conjugated with glutathione to reduce its toxicity to the body.
45
Q

Why does the adverse effects of NSAIDs occur in the GI system at lower doses than in other organ systems?

A

NSAIDs are weak acids that become lipid soluble in the highly acidic environment in the stomach → penetrate easily into gastric cells, and trapped in the relatively more alkaline environment
→ high local concentration of NSAIDs in the gastric mucosa

46
Q

What does prostaglandins normally do in the kidney?

A

The mesangial cells at the juxtaglomerular apparatus (JGA) in the kidney releases prostaglandins →
1) vasodilate the afferent renal arteriole to maintain renal blood flow and GFR
2) stimulate the release of renin from the juxtaglomerular cells

47
Q

What is the NSAIDs’ adverse effect for liver?

A

idiosyncratic effect

48
Q

What is the toxic dose for ibuprofen in dogs?

A

GI: 100-125 mg/kg
Renal: 175-300 mg/kg
CNS: 400 mg/kg
Death: 600 mg/kg

49
Q

Write down the elimination half-life for each NSAIDs.

A
50
Q

How do cats metabolize ketamine?

A

Kidney excretion

51
Q

True or False: Katamine has a direct negative cardiac inotropic effect.

A

True

Clinically, it is often overcome by CNS stimulation.

  • IV ketamine often causes increased pulmonary arterial pressure, heart rate, cardiac output, myocardial oxygen requirements, and cardiac work
52
Q

Can you use bupivacaine as IV to substitute lidocaine? Why?

A

No. IV Bupivacaine can cause severe cardiotoxicity

53
Q

How do you pick a reservoir bag?

A

5-10 times of patient’s tidal volume (10-20 ml/kg)

54
Q

What is the MOA for 𝜶2 agonist analgesic effect?

A

activation of 𝜶2a receptors → they are Gi protein-coupled voltage channel (K+) → activation leads to more of K+ leaving the cells → hyperpolarization

55
Q

In spinal cord, where are the majority of 𝜶2 receptors locate?

A

Dorsal horn of grey matter

56
Q

Where does NMDA antagonist’s analgesic effect happen?

A

Peripherally (dorsal horn of spinal cord; post-synaptically)
Supraspinally (limbic system, thalamoneocortical systems)

57
Q

Name the layers & spaces from the vertebral bone to spinal cord.

A

Epidural space
Dura mater
Subdura space
Arachinoid
Subarachinoid space
Pia mater

58
Q

Does subdura space contain CSF?

A

No
Subarachinoid space does

59
Q

What is the spinal innervation for caudal abdomen?

A

L3-S1

60
Q

What is the spinal innervation for pelvic limb?

A

L1-L3

61
Q

What is the spinal innervation for thorax?

A

T2-T13

62
Q

What is the spinal innervation for cranial abdomen?

A

T11-T13

63
Q

Why do we choose L7-S1 for epidural?

A

1) The intervertebral space is relatively wide
2) The landmark is easy to identify
3) The spinal cord and dura sac end at L6-L7 → less likely to penetrate the spinal cord and cause injury

64
Q

Describe how to perform epidural

A

1) Place the animal in sternal recumbency with both of the pelvic limbs gently pulled forward to open up the caudal intervertebral spaces
2) Identify the L7 spinous process. Clip and aseptically prepare the area for epidural injection.
3) Put on sterile glove. Identify the L7 spinous process and medial sacral crest. Insert a spinal needle caudal to the L7 spinous process. Make sure the needle is inserted at the mid line and is perpendicular to the skin.
4) Once the needle is advanced through the skin and into the subcutaneous tissue, gently advance the needle until the resistance is encountered.
5) Remove the stylet. A hanging drop is used to confirm the location of the needle tip. Gently fill the hub with sterile saline. Slowly advance the needle through the intervertebral ligament. Once the needle enter the epidural space, the saline should be suctioned into the epidural space. If bony structure is encountered, gently withdraw the need to the subcutaneous space and “walk” the needle caudally to find the intervertebral space. If there is any blood noticed in the hub, remove the entire spinal needle and a new needle should be used.
6) After the epidural space is correctly identified, administer the drug slowly over 1-2 minutes.
7) Gently withdrawal the needle

65
Q

What are the contraindication for epidural analgesia?

A

1) severe thrombocytopenia or coagulopathy
2) skin infection at the needle insertion site
3) known congenital malformation of the spine
4) Septic patient
5) Fracture of the LS area
6) Hypotensive or hemodynamically unstable patients (because epidural can also block the sympathetic trunk)
7) Known neurological deficit where the lesion localization is at the same area.

66
Q

What is the recommended volume for epidural block?

A

0.2 ml/kg (to achieve blockade up to L1)

  • If need to have cranial abdomen involved → 0.3 ml/kg
67
Q

What is the morphine dose for epidural. What is the duration?

A

0.1 mg/kg
6-24 hours

68
Q

True or False: Morphine epidural analgesia can cause patient unable to walk post-op up to 4 hours

A

False

Bupivacaine not morphine

69
Q

What is the recommended dose and concentration for bupivacaine?

A

0.5% 1-1.25 mg/kg

70
Q

What are the three opioids that can cause histamine release?

A

Morphine
Methadone
Meperidine

71
Q

What is the MLK formula if you want to put all the med in 1L of saline bag?

A

1) Remove 73ml of solution from the 1L saline bag
2) Add 68ml of 2% lidocaine, 4ml of Morphine (15 mg/ml) and 0.6ml of ketamine (100mg/ml) into the bag. Mix well and label it.
3) Run it at 1-2 ml/kg/hr

72
Q

Why diazepam CRI is not recommended in cats?

A

It contains propylene glycol which can cause severe metabolic acidosis

73
Q

List 5 other effects for 𝜶2 agonist besides sedation and analgesia.

A

1) cause hyperglycemia
2) inhibit antidiuretic hormone & renin release → promote diuresis and natriuresis
3) induce vomiting (cat)
4) decrease salivation
5) indirectly decrease cardiac output
6) sympatholysis

74
Q

is buprenorphine better absorbed in an acidic or basic environment when given transmucosally?

A

basic

75
Q

There are three types of 𝜶2 receptors, what are their main functions?

A

𝜶2a receptors (mainly in CNS): supraspinal analgesia, sedation, sympatholytic effect
𝜶2b receptors (vascular smooth muscle & spinal cord): vasoconstriction, spinal analgesia
𝜶2c receptors: mediating hypothermia

76
Q

List 4 adverse effects of lidocaine.

A

1) injection site pain
2) hypotension
3) seizure
4) vomiting

77
Q

What is normal DAP for dogs and cats?

A

90 mmHg

78
Q

What is the formula to calculate MAP based on SAP and DAP?

A

MAP = DAP + 1/3 (SAP-DAP)

ECVECC Board Exam (24 decks)

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