MAGA Exam II) Flashcards

1
Q

What are the 6 multimodal therapies discussed in lecture?

A
  • Periop Fluid
  • Carb loading
  • Short-acting Anesthetics
  • Opioid Sparing
  • Temp. Management
  • Cerebral/Neuromuscular monitoring
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The emphasis on Multimodal Anesthesia for general anesthesia includes which 2 aspects?

A

Short-acting anesthetics and opioid sparing

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

Define non-opioid anesthesia. List some alternatives to treat pain.

A

PT & OT, Chiropractic care, acupuncture, massage, yoga, weight loss, cold/heat, OTC medications, TENS unit…etc.

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

What is the pain response pathway? (5)

A

(this was in the pain pathway slide set too)

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

What are the 2 classes of opioids?

A

1) Phenanthrenes (L-isomers have opioid activity; morphine, codeine, thebaine)

2) Benzylisoquinolones (Lack opioid activity; Papaverine, noscapine)

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

Chart to memorize (per Dr. Castillo)

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

Using multimodal anesthesia, what 2 meds might we give in preop to better control pain later?

A

Acetaminophen 1000 mg PO, Gabapentin 300 mg PO

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

Regarding Gabapentin’s preemptive analgesia, What 3 studies/ procedures is it used in?

A
  • Spine surgeries
  • Orthopedic procedures
  • Major abdominal procedures.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

For Preemptive Gabapentin, what patient population is it contraindicated for?

A
  • MG and Myoclonus patients
  • Reduce dose in elderly patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the PO dose of preemptive Gabapentin?
When should we give it?
What is it’s MOA?

A

300-1200mg PO
1-2 hrs prior to OR
GABA analogue

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

What is the MOA of gabapentin?

A

GABA Analog actions:

  • Blockage of VG Ca⁺⁺ channels
  • inhibits release excitatory neurotransmitters
  • Descending inhibitory tract enhancement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Is gabapentin lipid soluble?
What percentage protein-binding occurs with gabapentin?
What’s it’s E 1/2 time?

A
  • Yes; Lipid soluble
  • not protein-bound (<3%)
  • Brief E 1/2 time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are Gabapentin’s side effects (7)?

A

Think ↑GABA effects

  • Somnolence
  • fatigue
  • ataxia
  • vertigo
  • GI disturbances: constipation
  • abrupt withdrawal in seizure pts (when Gaba is used as an antiepiliptic): causing seizures
  • wt gain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are indicated uses for gabapentin?

A
  • Partial seziures in adults and children
  • Neuropathic pain (DM Neuropathy, Neuralgias, Fibromyalgia, Phantom Limb)
  • Chronic pain syndromes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Does gabapentin have any drug-drug interactions?

A

No drug interactions

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

What are the 7 effects of NSAIDs discussed in lecture?

A
  • Decrease activation of peripheral nociceptors
  • No addictive potential
  • Preemptive analgesia
  • Absence of ventilatory depression
  • Less nausea and vomiting
  • Long duration of action
  • Absence of cognitive effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What enzyme catalyzes the synthesis of prostaglandins?

A

COX (Cyclooxygenase)

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

This form of COX is responsible for gastric protection, hemostasis, and renal function…

A

COX-1

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

COX-1 or COX-2?

Ubiquitous, “physiologic”, inhibition of this enzyme is responsible for many adverse effects.

A

COX-1

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

COX-1 or COX-2?

Pathophysiologic, expressed at sites of injury, not protective.

A

COX-2

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

COX-2 propagation is responsible for which symptoms?

A

Pain, inflammation, and fever

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

What are the three main properties of NSAID drugs?

A

Analgesic
Anti-inflammatory
Antipyretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Are the following drugs non-specific or COX-2 selective?

–Ibuprofen, naproxen, aspirin, and ketorolac–

What gastric symptomology would be seen with administration of these drugs?

A

Non-Specific
Increased gastric irritation with these drugs

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

Celecoxib (Celebrex), Rofecoxib (Vioxx), Valdecoxib (Extra), Parecoxib (Dynastat) are all examples of what?

A

COX-2 Selective NSAIDs

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

Do COX-2 selective NSAIDs affect platelets?

A

No, COX-1s do.

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

Because COX-2 selective NSAIDs have no effect on platelets, this would increase the chance of what pathology?

A

Clotting (think MI and CVA)

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

COX-2 selective and nonspecific inhibitors have _____________ analgesia

A

Comparable

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

What was the first COX-2 inhibitor that decreases PG synthesis?

A

Celecoxib (Celebrex)

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

What is the dosage for Celebrex?

A

200 to 400 mg PO QD

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

Celebrex reaches its peak in…

31
Q

For Ofirmev, what is the Dose, Peak effect time, and duration?

A

Dose is 3-4g max daily for testing purposes

32
Q

What kind of anti-inflammatory properties does Ofirmev have?

A

Trick question, none (or no significant effects)

33
Q

What contraindication(s) would you need to consider when prescribing Ofirmev?

A

Hepatic Impairment

34
Q

According to the TXWES medication guide, what are the doses for Acetaminophen (Ofirmev), Ketorlac (Toradol), & Ibuprofen (Caldor).

35
Q

What is the MOA for Ofirmev?

A

Reduces prostaglandin metabolites

36
Q

What are absolute contraindications for Ketorolac per Castillo?

A

Anaphylaxis reaction, Patient in Chronic Renal Failure (Not severe impairment), Low platelet count.

37
Q

For Ketorolac, what is the:

  • MOA
  • Peak
  • Dosing
A

MOA: Inhibits PG synthesis by inhibiting COX 1 and COX 2

Peak: 45 to 60 minutes IV

Dose: 15 to 30mg q6h (1/2 dose in elderly)
Max Dose: 60-120mg QD

38
Q

What are some contraindications to consider when giving Toradol?

A
  • Severe Renal impairment (not absolute C/I but needs to be heavily considered)
  • Renal Failure (For sure)
  • Risk for bleeding
  • CAD
  • CABG
  • Pregnant
  • NSAID allergy

Decrease dose (usually 1/2) for elderly: 15% loss in kidney function per decade after 50)

39
Q

Ibuprofen:

  • MOA
  • Contraindications
  • Dose
  • Peak
  • Excretion
A
  • COX 1 & 2 Inhibition = ↓ PG synthesis
  • Nephropathy, CABG, bleeding disorders, wound healing and esp. allergy!
  • 200 - 800 mg QD
  • 1-2 hours
  • Urine & Bile
40
Q

With non-opioid anesthesia, what medications are used for induction?

A

Propofol, Lidocaine, Ketamine, volatile anesthetics. Paralytic if needed.

41
Q

A 50 y/o, 60 kg female patient received a Lidocaine initial dose of 1 mg/kg with a subsequent infusion of 1.5 mg/kg/hour for 1.5 hours. How much total Lidocaine in mgs did she receive in the PACU?

A

60kg x 1 mg/kg = 60 mg
60 kg x 1.5 mg/kg = 90 mg (1 hour)
(60 kg x 1.5mg/kg = 90 mg)/2 = 45 mg (30 minutes)

60+90+45 = 195 mg total!!!

42
Q

Multidose lidocaine vials are used for _____.

A

infiltration or peripheral nerve block.

43
Q

Lidocaine is an ______ structure local anesthetic.

Which drug is an exception to the amide/ester rule?

A
  • Amide (amides anesthetics have 2 “i”s)
  • Cocaine. Cocaine is also local amide anesthetic.
44
Q

How is lidocaine metabolized?

45
Q

What is the IV bolus and infusion dose of lidocaine?
When should the infusion be terminated?

A
  • 1 to 2 mg/kg IV bolus over 2-4 min.
  • 1 to 2 mg/kg/hr infusion
  • Terminated within 12-72 hours.
46
Q

Lidocaine plasma concentration of ____ causes what?

1-5 mcg/ml = ?

5-10 mcg/ml = ?

A

1-5 = analgesia

5-10 = circum-oral numbness; tinnitus; skeletal muscle twitching; systemic HYPOtension; myocardial depression

47
Q

Lidocaine plasma concentration of ____ causes what?

10-15 mcg/ml = ?

15-25 mcg/ml = ?

A

These are OD levels

10-15 = Sz’s; unconsciousness

15-25 = apnea (pons & medullary depression); coma

48
Q

If we give Lido w/ Epi, should the dose be higher or lower?
Why?

A

Higher: epinephrine will locally vasoconstrict and prevent lidocaine leakage into the intravascular space.

(Castrater)

49
Q

How is lidocaine overdose treated?

A

Lipid rescue

50
Q

What is one of magnesium’s primary MOAs (for this pharm class)?

A

N-methyl-D-aspartate (NMDA) receptor
antagonist
- Probably potentiates opioids centrally
and peripherally

51
Q

Mg++ regulates which four cellular functions?

A
  • Ca++ access intracellularly.
  • Neurotransmission
  • Cell signaling
  • Enzyme function
52
Q

Which patients receive magnesium sulfate most often per Castillo?

A

Preeclamptic & eclamptic OB patients.

53
Q

This med has anti-nociceptive effects by antagonizing the NMDA receptor and “probably” potentiates opioids centrally and peripherally.

54
Q

Which ion has limited movement across the BBB?

55
Q

What conditions are contraindicative for magnesium administration?

A

Myasthenia Gravis & Renal Failure

56
Q

What adverse side effects could occur with Mg++?

A

Hypotension, bradycardia, ataxia, somnolence, decreased muscular tone.

57
Q

What is Mg⁺⁺ dosing for the following two situations?

Preop:
Intraop:

A
  • Preop: 50 mg/kg IV
  • Intraop: 8 mg/kg/hr IV

Be prepared to treat bradycardia and/or hypotension

58
Q

What opioid requirement does the use of Mg++ significantly decrease?

A

Fentanyl

It is thought that Mg++ potentiates opioids both centrally and periphreally

59
Q

What drug class does Ondansetron fall into?
What was it first developed for?
What CYP450 is relevant to ondansetron?

A

It is the first 5-HT3 antagonist
-It was approved for CINV
-Responsiveness decreased by variations in the CYP2D6 activity!

60
Q

Ondansetron is equivocal to what two drugs in its treatment of N/V?

A

Droperidol & Metoclopramide

61
Q

What are the side effects of Ondansetron?

A
  • HA
  • Constipation
  • Possible QT prolongation if given rapidly so give it slowly!!
62
Q

What is the duration & dose of Ondansetron?

A

Duration/plasma half life is 4 hours!
Dose: Adults: 4 mg IV (up to 8 mgs)
Dose: Pediatrics: 0.1 mg/kg IV

63
Q

What is the MOA of Corticosteroids in the treatment of N/V?

Why are Corticosteroids used with 5-HT3 (Ondansetron) & droperidol?
Hint: It was studied in CINV!

A
  • MOA is unknown: It works on glucocorticoid receptors in Nucleus Tractus Solitarius (NTS).
  • Corticosteroids potentiate 5 HT3 antagonists and droperidol!
64
Q

What is the dose for Dexamethasone (Decadron)?

What is the MOA of Dexamethasone (Decadron)?

A

4 - 10 mg IV

MOA: Anti-inflammatory; inhibition of phospholipase and cytokines and stabilization of cellular membrane.

65
Q

What is the delay of onset of Dexamethasone (Decadron)? How long does efficacy persist?

Are there any adverse effects of a single dose of Dexamethasone (Decadron)?

What occurs if it is pushed fast?

A
  • Onset: 2 hours. Efficacy: 24 hours.
  • Nope (proven safe even in DM population)
  • Perineal burning/itching (usually D/T rapid inj)
66
Q

What is the MOA of Precedex (Dexmeditomidine)?
How does it compare to Clonidine?

A
  • Highly selective (7-10x more than Clonidine), specific (pontine locus coeruleus), potent, and full α2 adrenergic agonist.
  • Clonidine is only a partial agonist
  • Shorter duration of action vs. Clonidine
67
Q

Can we reverse Precedex (Dexmedetomidine)?

A

Yep, Atipamezole antagonizes Precedex so that’s nice.

68
Q

What are the primary uses for Precedex (Dexmedetomidine)?

A
  • Concious Sedation: Calmness, easily rousable, spontaneous ventilation, amnesia is ** not** assured. Also good in Postop/ICU
  • General Anesthesia: Tracheal intubation and allows for decreased perioperative requirements of inhaled anesthetics & opioids.
  • TIVA: Depression of ventilation
69
Q

For Precedex, state the following:
- Half-time
- Metabolism/Excretion
- It is a weak ___ of CYP450
- Can cause ___tension in high doses and ___cardia with rapid infusion (also high doses)

A
  • 2-3hours (Clonidine=6-10)
  • Hepatic/Renal
  • Inhibitor
  • Hypo/Brady
70
Q

What are the TIVA/GA doses for Precedex?

A
  • Bolus 0.5-1 μg/kg, over 10 mins
  • High Dose
    Loading dose of 1 μg/kg, then 5-10 μg/kg/hour IV
    0.1-1.5 μg/kg/min infusion
71
Q

What is the sedation dose for Precedex?
How about IV Regional?

A
  • 0.2-0.7 μg/kg/hour IV
  • 0.5 μg/kg with lidocaine
72
Q

What is the neuraxial dose for Precedex?

A
  • Spinal/Intrathecal/SAB: 3 μg (as combo), 5 μg with Fentanyl, or 25 μg (alone)
  • Epidural: 2 μg/kg

We really don’t see this in practice according to Dr. Castillo. Just give IV.

73
Q

Precedex can decrease the need for inhaled anesthetics & opioids by up to ___%