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APEX > Pharm > Flashcards

Pharm Flashcards

1
Q

What ↑ risk of LAST?

A
  • Hypercarbia (↑ CBF → more drug → brain)
  • Hyperkalemia (↑ RMP)
  • Metabolic acidosis
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2
Q

Max dose lidocaine for tumescent

A

55mg/kg

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3
Q

Max dose chlorprocaine

A

Plain chlorprocaine: 11mg/kg, 800mg total

With epi: 14mg/kg, 1000mg total

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4
Q

What is clearance directly proportional to? Inversely proportional to?

A

Clearance is directly proportional to:
→ blood flow to clearing organ
→ extraction ratio
→ drug dose

Clearance is inversely proportional to:
→ half-life
→ drug [] in central compartment

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5
Q

Longest context-sensitive half times of opioids

A

Fentanyl (by a mile)
Alfentanil
Sufentanil
Remi is flat -

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6
Q

How to tell if a drug is a weak acid or base by its name

A

A weak acid is paired with a + ion such as sodium, calcium, Mg
→ Sodium thiopental

A weak base is paired with a (-) ion such as chloride or sulfate
→ Lidocaine hydrochloride
→ Morphine sulfate

Etc etc

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7
Q

→ of ↓ plasma proteins

A

Liver disease, renal disease, old age, malnutrition, pregnancy, neonates

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8
Q

Zero order kinetic drugs

A

ETOH, ASA, phenytoin, Warfarin, heparin, theophylline

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9
Q

Drugs who undergo perfusion dependent hepatic elimination

A 
Fentanyl
Lidocaine
Propofol
Sufentanil
Ketamine
Bupivicaine
Metoprolol
Propranolol

HBF greatly exceeds enzymatic activity

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10
Q

Drugs that undergo capacity-dependent hepatic elimination

A 
Roc
Diazepam
Lorazepam
TPL
Phenytoin

Changes in hepatic enzyme activity or protein binding have profound effects on these drugs (ER <0.3)

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11
Q

Differences in drug excretion with basic and acidic urine

A

Basic urine favors
→ reabsorption of basic drugs
→ excretion of acidic drugs

Acidic urine favors
→ reabsorption of acidic drugs
→ excretion of basic drugs

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12
Q

Drugs eliminated by nonspecific esterases

A

Remi, esmolol, etomidate (partially), atracurium (partially)

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13
Q

Therapeutic index

A

LD50/ED50

LD50=lethal in 50% population
ED50=effect in 50% population

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14
Q

Racemic mixtures

A

Ketamine, morphine, iso, des, bupivicaine, methohexital, TPL, methadone, toradol

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15
Q

Protein binding numbers for IV anesthetics

A

Propofol 98%
Midaz, precedex 94%
Etomidate 75%
Ketamine 12%

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16
Q

Which opioid is naloxone not that effective in reversing?

A

Buprenorphine. Binds to the mu receptor with an affinity 50x greater than morphine. It’s also v slow to dissociate from the receptor. For these reasons, it is highly resistant to competitive antagonism by Narcan.

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17
Q

Things that prolong the half life of drugs dependent on hepatic metabolism

A

-↓ drug delivery to liver
→ CHF

  • ↓ hepatic metabolism
    → cirrhosis
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18
Q

What do pKA, lipid solubility, and protein binding correlate to in terms of LAs?

A

PKA → onset
Lipid solubility → potency
Protein binding → DOA

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19
Q

Drugs that can mess with pseudocholinesterase

A 
Neostigmine 
Echothiopate
Metoclopramide
Esmolol
BCP/estrogen
Cyclophosphamide
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20
Q

Things that ↑ FA/FI → faster onset of inhaled agent

A

↓ uptake: low solubility of agent (think des)
↓ CO (hypothyroidism)

↑ Wash in: High FGF, High Aleveolar ventilation, low FRC, Low Vd

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21
Q

Things that decrease FA/FI → slow down onset of inhaled agent

A

↑ UPTAKE

↑ solubility (think iso)
↑ CO
 ↑ Pa-Pv difference
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22
Q

Vessel rich group

A

75% CO, 10% body mass

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23
Q

Muscle and skin

A

20% CO, 50% body mass

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24
Q

Fat

A

5% CO, 20% body mass

25
Q

Hepatic biotransformation of IAs

A

N20: 0.004%
Des: 0.02%
Iso: 0.2%
Sevo: 2-5%

Alphabetical order (D-I-S) and “rule of 2’s (.02, .2, 2)”

26
Q

How does soda lime contribute to the breakdown of halogenated anesthetics?

A

Sevo → compound A when exposed to soda lime, worse when dry

Des + iso → CO in presence of dry soda lime

Important to know that TFA and free fluoride ions are produced during biotransformation inside the body, while compound A and CO are produced following exposure to soda lime outside the body.

27
Q

Concentrating effect

A

When pt breathes room air, plain nitrogen is primary gas in alveolus, but n20 is 34x more soluble in blood than plain nitrogen.

When N20 introduced into lung, volume of N20 going from alveolus → pulmonary blood is much higher than amount of nitrogen moving from pulmonary blood → alveolus. This → the alveolus to shrink and the reduction in alveolar volume → ↑ FA.

The concentrating effect explains why N20 (not des) has the highest FA/FI curve even tho des is less soluble in blood. Simply put, the sheer volume of N20 movement more than compensates for the small difference in blood solubility.

28
Q

Augmented gas inflow effect

A

Concentrating effect temporarily reduces alveolar volume.

On subsequent breath, the concentrating effect → ↑ inflow of tracheal gas containing anesthetic to replace the lost alveolar volume, this ↑ alveolar volume and further hastens FA. Alveolar volume is restored quickly so this phenomenon is short lived.

29
Q

Diffusion hypoxia

A

Related to second gas effect

Gas containing areas of body can absorb up to 30L of N20 within 2 hrs, but most is eliminated within 5 mins when you turn nitrous off. As this huge volume of nitrous is transferred back into the alveoli, it dilutes alveolar 02 and C02, can cause a temporary diffusion hypoxia and hypercarbia.

Giving 100% Fi02 for 5 min when you kill the nitrous will stop this

30
Q

How is anesthetic gas onset affected by R → L shunting?

…what about IV agent onset?

A

Slows down FA/FI.

The FA/FI of an agent with lower solubility will be more affected, (think des). More soluble agents (like iso) experience more uptake from blood so that kinda offsets the R → L shunt dilution effect.
Less soluble agents like des undergo very little uptake by blood so the shunt’s dilutional effect is left unchecked.

Therefore…desflurane is affected the most, iso the least.

For IV, a R → L shunt produces faster onset (blood bypasses lungs and travels towards brain faster).
Also for IV, L → R shunt slows down IV induction (agent is recirculated in the lungs). L → R shunt has no real effect on FA/FI

31
Q

Examples of R → L shunts

A 
Tetralogy of Fallot
Foramen ovale
Eisenmergers 
Tricuspid atresia
Ebstein’s anomaly
32
Q

Ocular gas bubble placement and N20 D/C

A

DC N20 15 mins before SF6 placed, don’t use for 7-10 days after

Air bubble: avoid N20 5 days
Perfluoropropane: avoid N20 30 days
Silicone oil is fine

33
Q

VA action in spinal cord

A

In spinal cord, IAs produce immobility in the ventral horn. Sites:
→ glycine receptor stimulation
→ NMDA receptor inhibition
→ Na+ channel inhibition

GABA-A stimulation has nothing to do with immobility, since its only in the brain.

34
Q

Which inhalational agent theoretically does not affect HR at all?

A

Sevo

All others cause ↑

35
Q

Which agent theoretically ↓ BP the most?

A

Iso

36
Q

Effect of IAs on peripheral chemoreceptors

A

Peripheral chemoreceptors monitor for hypoxemia (respond to 02 rather than C02)

VAs impair periph chemoreceptors for up to several hrs after

Impaired response to HYPOXIA (not hypercarbia) occurs at 0.1MAC

37
Q

Which agent impairs hypoxic drive the least

A

Desflurane

Best in patients who rely on hypoxic drive to breathe (emphysema, sleep apnea)

38
Q

PKAs of LAs

A 
Mepivicaine 7.6
Lidocaine, Prilocaine 7.9
Ropivicaine, Bupivicaine 8.1
Tetracaine 8.5
Chlorprocaine 8.7
Procaine 8.9
39
Q

Areas of highest vascular uptake to lowest for LAs

A 
IV
Tracheal
Interpleural
Intercostal
Caudal
Epidural
Brachial
Femoral
Sciatic
Sub-q
40
Q

Max dose bupivicaine

A

2.5mg/kg or

175mg total

WITH EPI: 3mg/kg, 200mg total

41
Q

Max dose lidocaine

A

4.5mg/kg, or 300mg total

WITH EPI: 7mg/kg, 500mg total

42
Q

Max dose ropivicaine

A

3mg/kg or

400mg total

43
Q

Max dose prilocaine

A

8mg/kg or 500-600mg total

44
Q

Max dose cocaine

A

3mg/kg not to exceed 200mg

45
Q

Dose of lipid rescue for LAST

A

20% 1.5mL/kg bolus over 1 min

Infusion 0.25mL/min

46
Q

Drugs to AVOID when treating LAST

A
  • Propofol (augments myocardial depression even tho it might break the seizure)
  • Beta blockers or calcium channel blockers
  • Lidocaine (duh)
  • Epi, vasopressin

Can give sux to ↓ 02 demand of seizure even tho it wont actually break the seizure, amiodarone for ACLS

47
Q

Dibucaine number

A

20: atypical homozygous, sux duration 4-8 hrs

50-60: heterozygous, sux durations 20-30min

Normal is 80

48
Q

Drugs that cause prolong QT interval

A 
Methadone
Droperidol
Haloperidol
Ondansetron
Halogenated anesthetics
Amiodarone 
Quinidine
49
Q

Which conditions slow down FA/FI rise or speed of induction?

A

Anything that ↑ CO (↑ temp, ↑ BMR)

↑ FRC

50
Q

Mu-1

A 
Analgesia (SS and spinal)
Bradycardia
Euphoria
Low abuse potential
Mitosis
Hypothermia
Urinary retention
51
Q

Mu-2

A

Analgesia (spinal only)
Resp depression
Constipation
Physical dependence

52
Q

IM ketamine dose

A

4-6mg/kg

53
Q

Drugs with NMDA antagonistic activity

A 
N20
Ketamine
Methadone
Mg
Dextromethorpan
xenon
54
Q

Equivalent dose of intrathecal morphine for epidural

A

Intrathecal morphine 0.25-3mg is equivalent to epidural morphine 2-5mg

55
Q

Inhibitors of CYP3A4

A

(Metabolizes fentanyl)

-Grapefruit juice, ketoconazole, erythromycin

56
Q

Sugammadex dosing

A

Dosed on TBW

57
Q

Drugs to avoid with porphyria

A 
Barbiturates
Sulfa
Alcohol
Diazepam
Phenytoin
Nifedipine
Etomidate
Ketorolac
Glucocorticoids
Hydralazine
58
Q

What does the dibucaine number actually reflect

A

Dibucaine is an amide LA that inhibits normal plasma cholinesterase, but doesn’t affect atypical PChE. The number is the percentage of normal enzyme that is inhibited by dibucaine, so higher is more normal, lower is more abnormal

APEX (11 decks)

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