Exam 2 Dr. Castillo Key Points Flashcards

1
Q

What are barbiturates known as in anesthesia?

A

The gold standard of anesthesia.

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

How do barbiturates affect GABA-A channel activity?

A

They potentiate GABA-A channel activity.

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

What can prolonged infusion of barbiturates lead to?

A

Lengthy context sensitive half time.

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

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

What are the primary characteristics of thiopental?

A
  • Rapid redistribution (Calculate based on IBW)
  • significantly more lipid soluble then oxybarbiturates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the side effects associated with methohexital?

A

Myoclonus, hiccups.

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

What receptors does propofol act on?

A

GABA-A receptors to increase chloride conductance.

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

What is the metabolism pathway for propofol?

A

CYP450 metabolism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a sub-hypnotic dose of propofol?

A

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

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

What is a notable effect of propofol on respiratory resistance?

A

It acts as a bronchodilator and decreases respiratory resistance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

myoclonus

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

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

A

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

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

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

A
  • BRADYCARDIA
    Blackbox warning for profound bradycardia and asystole with healthy adult patients (consider glyco administration before propofo, especiallyif giving to pedi)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A
  • dose
  • intact
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How are liver enzymes typically in patients on propofol?

A

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

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

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

A

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

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

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

A

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

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

What are common side effects of etomidate?

A
  • High incidence of myoclonus.
  • Pain on injection/venous irritation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Etomidate MOA

A

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

20
Q

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

A
  • 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.
21
Q

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

A

It is cardiac safe but does not produce analgesia.

23
Q

What does etomidate suppress?

A

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

24
Q

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

A
  • constrictor
  • decreased
  • 35-45%
25
Q

What type of pain does ketamine provide?

A

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

26
Q

What receptors does ketamine bind to?

A
  • Non-competitively to NMDA receptors (decreases glutamate release).
  • Also binds to opioid (μ, δ, and κ; weak σ)
  • weak action at GABA-A receptors
27
Q

What is the onset and duration of action for ketamine?

A
  • 1 minute
  • 15-20 minutes.
  • 60-90min full orientation and amnestic effect
28
Q

What can be used to manage ketamine-induced salivation?

A

Glycopyrrolate>atropine

29
Q

What is the CAD cocktail?

A
  • Diazepam 0.5 mg/kg IV
  • Ketamine 0.5 mg/kg IV
  • Continuous Ketamine infusion: 15 to 30 μg/kg/minute IV
30
Q

What are the four processes involved in pain pathways?

A
  • 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.)
31
Q

What is the role of the thalamus in pain perception?

A

Acts as the central relay station for incoming pain signals.

32
Q

What types of fibers are involved in nociceptive signaling?

A
  • Unmyelinated - C fibers
  • Myelinated - A fibers
33
Q

What are some chemical mediators involved in pain?

A
  • Peptides (Substance P, Calcitonin, Bradykinin)
  • Lipids (Prostaglandins, Thromboxanes, Leukotrienes, Endocannabinoids)
34
Q

What does the Gate Control Theory describe?

A

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

35
Q

What types of impulses can modulate pain?

A
  • Excitatory Impulses (Glutamate, Calcitonin, Neuropeptide Y, Aspartate, Substance P)
  • Inhibitory Impulse (Glycine, GABA, Enkephalins, Norepinehrine, Dopamine)
36
Q

What are the types of ascending pathways involved in pain?

A
  • Spinothalamic
  • Spinomedullary
  • Spinobulbar
  • Spinohypothalamic
37
Q

What is the mechanism of action for opioids?

A

Presynaptic inhibition of neurotransmitters and increased K conductance.

38
Q

What is the gold standard of opioids?

39
Q

What is a significant side effect of opioids?

A

Constipation.

40
Q

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

A

Greater than sufentanil.

41
Q

What do opioid agonist-antagonists do?

A

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

42
Q

What is the primary use of buprenorphine?

A

Post-operative pain management.

43
Q

What is the effect of multimodal drugs like gabapentin?

A

Enhances descending inhibition and inhibits excitatory transmitter release.

44
Q

What are the types of NSAIDs mentioned?

A
  • Non-Specific (Ibuprofen, Naproxen, Aspirin)
  • COX-2 selective (Celecoxib, Rofecoxib, Valdecoxib)
45
Q

What is the effect of magnesium in pain management?

A

NMDA receptor antagonist.