Exam 2 Dr. Castillo Key Points

Question 1

What are barbiturates known as in anesthesia?

Answer 1

The gold standard of anesthesia.

Question 2

How do barbiturates affect GABA-A channel activity?

Answer 2

They potentiate GABA-A channel activity.

Question 3

What can prolonged infusion of barbiturates lead to?

Answer 3

Lengthy context sensitive half time.

Barbiturates rapidly redistribute from brain to other tissues; VRG to tissues

Question 4

What are the primary characteristics of thiopental?

Answer 4

• Rapid redistribution (Calculate based on IBW)
• significantly more lipid soluble then oxybarbiturates

Question 5

What are the side effects associated with methohexital?

Answer 5

Myoclonus, hiccups.

Question 6

What receptors does propofol act on?

Answer 6

GABA-A receptors to increase chloride conductance.

Question 7

What is the metabolism pathway for propofol?

Answer 7

CYP450 metabolism.

Question 8

What is a sub-hypnotic dose of propofol?

Answer 8

10-15mg IV followed by 10 mcg/kg/min.

Question 9

What is a notable effect of propofol on respiratory resistance?

Answer 9

It acts as a bronchodilator and decreases respiratory resistance.

Question 10

What happens to cerebral blood flow (CBF) and CMRO2 with large doses of propofol?

Answer 10

Decreases CBF and CMRO2 concurrently (coupled) and large doses may decrease cerebral perfusion pressure
- Make sure to support MAP.

Question 11

While propofol does not induce seziures, it can cause ___, which might look like a seziure.

Answer 11

myoclonus

Question 12

Compared to thiopental, what is propofol’s effect on BP?

Answer 12

SBP drop is greater than thiopental’s transient drop.
- Inhibition of SNS leads to vascular smooth muscle relaxation,↓ SVR, and ↓ ICF Ca++.
- Can modulate with laryngoscopy stimulus (cold blade=excitation)
- Hypovolemia is exaggerated in elderly and patients with LV compromise

Question 13

What other issues occur with the decreases in SNS response after administering propofol?

Answer 13

• BRADYCARDIA
  Blackbox warning for profound bradycardia and asystole with healthy adult patients (consider glyco administration before propofo, especiallyif giving to pedi)

Question 14

Propofol causes a ____-dependent depression of ventilation but leaves patients with a(n) ___ hypoxic pulmonary vasoconstriction response

Answer 14

• dose
• intact

Question 15

How are liver enzymes typically in patients on propofol?

Answer 15

Intact and creatanine is normal
- Prolonged infusion can cause hepatocellular injury and/or propofol infusion syndrome with NO CHANGE TO CREATININE, even with cloudy urine

Question 16

What syndrome can prolonged infusion of propofol cause? What is the dosing/timing structure?

Answer 16

Propofol infusion syndrome (lactic acidosis, brady-dysrhythmias, rhabdo.
>75mcg/kg/min for more than 24hrs
- this is reversible in early stages but can lead to cardiogenic shock and require ECMO in later stages

Question 17

What is a significant risk of propofol infusion syndrome in children?

Answer 17

Fatal bradycardia.
-Pre-treat with glyco to maintain their HR

Question 18

What are common side effects of etomidate?

Answer 18

• High incidence of myoclonus.
• Pain on injection/venous irritation

Question 19

Etomidate MOA

Answer 19

Indirectly opens GABA-A receptor Cl- channels
- cell hyperpolarization

Question 20

How is etomidate metabolized? Excreted? What is the peak effect time for etomidate?

Answer 20

• Metabolized vis hepatic microsomal enzymes and plasma esterases (great for renal/liver patients?)
• Eliminate in urine (85%) and bile (10-13%
• Peaks in 2 minutes.

Question 21

What is our favorite thing about etomidate? What don’t we like about it?

Answer 21

It is cardiac safe but does not produce analgesia.

Question 23

What does etomidate suppress?

Answer 23

Stress response
- severe hypotension, use with caution in sepsis and hemorrhage due to need of catecholamines and stress response for bp

Question 24

Etomidate is a potent cerebral vaso____. This leads to ____ ICP. It can also decrease CBF and CMRO2 by ____%.

Answer 24

• constrictor
• decreased
• 35-45%

Question 25

What type of pain does ketamine provide?

Answer 25

Profound analgesia (both the drug and the preservative, benzethonium chloride) - no pain on injection either

Question 26

What receptors does ketamine bind to?

Answer 26

- Non-competitively to NMDA receptors (decreases glutamate release). - Also binds to opioid (μ, δ, and κ; weak σ) - weak action at GABA-A receptors

Question 27

What is the onset and duration of action for ketamine?

Answer 27

- 1 minute - 15-20 minutes. - 60-90min full orientation and amnestic effect

Question 28

What can be used to manage ketamine-induced salivation?

Answer 28

Glycopyrrolate>atropine

Question 29

What is the CAD cocktail?

Answer 29

* Diazepam 0.5 mg/kg IV * Ketamine 0.5 mg/kg IV * Continuous Ketamine infusion: 15 to 30 μg/kg/minute IV

Question 30

What are the four processes involved in pain pathways?

Answer 30

* Transduction (Nerve/electrical impulses/signal start at the nerve endings) * Transmission (Travel of nerve/electrical impulses to the nerve body connecting to the dorsal horn of the spinal cord.) * Modulation (Process of altering (inhibitory/excitatory) pain transmission mechanisms at the dorsal horn to the PNS and CNS.) * Perception (Thalamus acting as the central relay station for incoming pain signals & the primary somatosensory cortex serving for discrimination of specific sensory stimuli.)

Question 31

What is the role of the thalamus in pain perception?

Answer 31

Acts as the central relay station for incoming pain signals.

Question 32

What types of fibers are involved in nociceptive signaling?

Answer 32

* Unmyelinated - C fibers * Myelinated - A fibers

Question 33

What are some chemical mediators involved in pain?

Answer 33

* Peptides (Substance P, Calcitonin, Bradykinin) * Lipids (Prostaglandins, Thromboxanes, Leukotrienes, Endocannabinoids)

Question 34

What does the Gate Control Theory describe?

Answer 34

The opening and closing of gates in the spinal cord that affect pain perception.

Question 35

What types of impulses can modulate pain?

Answer 35

* Excitatory Impulses (Glutamate, Calcitonin, Neuropeptide Y, Aspartate, Substance P) * Inhibitory Impulse (Glycine, GABA, Enkephalins, Norepinehrine, Dopamine)

Question 36

What are the types of ascending pathways involved in pain?

Answer 36

* Spinothalamic * Spinomedullary * Spinobulbar * Spinohypothalamic

Question 37

What is the mechanism of action for opioids?

Answer 37

Presynaptic inhibition of neurotransmitters and increased K conductance.

Question 38

What is the gold standard of opioids?

Answer 38

Morphine.

Question 39

What is a significant side effect of opioids?

Answer 39

Constipation.

Question 40

What is the context-sensitive half-time of fentanyl?

Answer 40

Greater than sufentanil.

Question 41

What do opioid agonist-antagonists do?

Answer 41

Bind to Mu, kappa, delta receptors with partial effects. - These partial effects act like an antagonist to other opioids

Question 42

What is the primary use of buprenorphine?

Answer 42

Post-operative pain management.

Question 43

What is the effect of multimodal drugs like gabapentin?

Answer 43

Enhances descending inhibition and inhibits excitatory transmitter release.

Question 44

What are the types of NSAIDs mentioned?

Answer 44

* Non-Specific (Ibuprofen, Naproxen, Aspirin) * COX-2 selective (Celecoxib, Rofecoxib, Valdecoxib)

Question 45

What is the effect of magnesium in pain management?

Answer 45

NMDA receptor antagonist.