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Anesthesia 101 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

All ester LA are metabolized by ______

A

hydrolysis by pseudocholinesterase

*just like succinylcholine

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2
Q

Succinylcholine is metabolized by _____

A

pseudocholinesterase

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3
Q

What drugs are metabolized by pseudocholinesterase?

A
  1. Succinylcholine
  2. ester LA
  3. Cocaine
  4. Heroin

*A pseudocholinesterase deficiency will prolong the effects of the drug

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4
Q

What promotes more bradycardia, high dose or repeated doses of succinylcholine?

A

Repeat dosing

*dose > 6mg/kg produces a phase 2 block

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5
Q 
Prolonged immobilization (after ~16 days) results in upregulation of immature AChRs.
- Response to succinylcholine?
A

Hyper sensitivity

  • Succ is easily able to interact with these receptors
  • Substantial efflux of K (lethal)
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6
Q

Do anticholinergic toxicity present with diaphoresis?

A

No the cause of hyperthermia is lack of perspiration

- Thyroid storm also presents with hyperthermia, but will be diaphoretic

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7
Q

Most anesthetic drugs are cleared by the (kidney / liver)

A

liver transformation

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8
Q

Best depth for TEE probe?

A

T5-T6 mid thoracic spine

- 30-35 cm

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9
Q

Enoxaparin is a LMWH that binds and potentiates ______ , which will prolong (PTT / PT)

A

antithrombin to irreversibly inactivate factor Xa.

PTT

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10
Q

Unfractionated heparin binds and potentiates _____

A

antithrombin III, which in turn inhibits factor II (thrombin) and Factor Xa

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11
Q

Dabigatran is a ______, that leads to increases in (PT / PTT)

A

Direct thrombin inhibitor

both PT and PTT

*No therapeutic monitoring in place

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12
Q

Rivaroxaban is a ______, that leads to increase in (PT / PTT)

A

direct factor Xa inhibitor

Both PT and PTT

*monitor using anti-Xa levels

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13
Q

(True / False) Acute herpes zoster treatment, acyclovir, prevents future herpes recurrence

A

False

- its only effective as a prophylaxis if CHRONIC treatment, not acute.

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14
Q

Droperidol is contraindicated in any pt with ______

A

prolonged QT

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15
Q

The half-life of aminoamide LA is prolonged in (ESRD / End stage liver disease)

A

Liver disease

  • hepatic enzyme dysfunction
  • or immature enzymes in neonates
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16
Q

Why is bupivacaine not used for IV regional anesthesia?

A

High risk of LA toxicity and death

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17
Q

Absolute contraindication to propofol

A

Hypersensitivity to egg lecithin/phosphatide (yolk), soy products

*most people are allergic to egg white (egg albumin)

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18
Q

Can neuraxial opioids lead to tolerance, requiring a dosage escalation to obtain same response?

A

Yes

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19
Q

Why do infusion rates of remifentanil need to be cut in 1/3 in elderly pts?

Why do bolus doses of opioids need to be halved?

A

Decreased central clearance
- inc opioid effectiveness

Decreased central volume of distribution

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20
Q

The maximum dose of lidocaine with and without epi is ____.

Epi [ ] in a LA should not exceed:

A

Without: 5mg/kg
With: 7mg/kg

1:200,000

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21
Q

A phase II block is a result of _______with ongoing cellular sodium and potassium shifts ultimately rendering the receptor unresponsive to further binding by ACh

A

Hyperactivation of ACh receptors

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22
Q

Volatile anesthetics cause muscle relaxation through ______

A

inhibition of ACh receptor sensitivity and hyperpolarization of motor neurons

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23
Q

Citrate intoxication can occur with blood transfusion and may present as a metabolic (acidosis/alkalosis)

A

alkalosis

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24
Q

NNT for:
Dexamethasone:
Ondansetron:
Droperidol:

A

Dexamethasone: 4
Ondansetron: 3
Droperidol: 5

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25
Q

GABA is an (Excitatory/Inhibitory) neurotransmitter that controls the state of chloride ion channels.
- How does this contribute to muscle relaxing properties?

A

Inhibitory
- Activation of Cl- channels -> neuronal hyperpolarization -> decreases ability for membrane potential to occur

*BDZ facilitate GABA receptors (inhibitory) in the CNS (CENTRAL)

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26
Q

Midazolam bioavailability by route of administration from greatest to least

A 
IV
SubQ
IM
Sublingual
Intranasal
Rectal (20-50%)
Oral
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27
Q

Concurrent use of antacids or grapefruit can (increase/decrease) the onset time and bioavailability of midazolam

A

Increase

by inhibiting the Cyt P450 enzyme system

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28
Q

_____ has the lowest cardiac-to-CNS dose toxicity ratio (2:1)

*ratio of dose causing cardiac collapse to dose causing seizures/convulsions

A

Bupivacaine

  • and the HIGHEST relative potency for cardiac toxicity
  • d/t stronger affinity for both resting and inactivated sodium channels w/in myocardium

*Ropivacaine has same cardiac-to-CNS dose toxicity ratio (2:1), but less cardiac toxicity

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29
Q

Do you need to monitor anti-factor Xa levels to predict safe neuraxial placement?

A

no

- not predictive of bleeding risk unless elderly pt with renal insufficiency receiving therapeutic doses of LMWH

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30
Q

Which one affects PTT more, LMWH or unfractionated heparin?

A

Unfractionated heparin

*do not need to routinely monitor PTT in pts on LMWH, it is highly predictable

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31
Q

(LMWH / Unfractionated heparin) prolongs PTT to a larger extent

A

Unfract. Hep.

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32
Q

What is the dosing for lipid emulsion (20%) in pts with LAST?

A

bolus 1.5ml/kg over 1 min

infusion 0.25 ml/kg/mi

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33
Q

What is the preferred treatment of arrhythmias in pts with LAST?

A

amiodarone

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34
Q

How is the dose of epi changed in ACLS if LAST is suspected?

A

dose < 1 mcg/kg per dose

- epi is arrhythmogenic in itself and make LAST more pronounced

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35
Q

The maximum allowable dose of lidocaine:

  • without epi
  • with epi
A
  • without epi: 5mg/kg
  • with epi: 7mg/kg
    over 60 min

1% lidocaine = 10mg/mL
2% lidocaine = 20mg/mL

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36
Q

The maximum allowable dose of bupivacaine:

  • without epi
  • with epi
A
  • without epi: 2.5mg/kg
  • with epi: 3mg/kg
    over 120min
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37
Q

What is the maximum allowable dose of 2% lidocaine (20mg/mL) with epi in a 70kg pt?

A

7mg/kg * 70kg = 490mg

490mg / (20mg/mL) = 24.5 mL

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38
Q

When the pH of the soln is LESS than the pKa, the molecule will be (ionized/unionized) at physiologic pH

A

ionized

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39
Q

When the pH of the soln is EQUAL to the pKa, the molecule will be (ionized/unionized)

A

both
50% ionized
50% unionized

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40
Q

What happens when bicarbonate is added to local anesthetics? downside?

A

increases the non-ionized form of lidocaine
- increases speed of onset

  • can form precipitation
  • unionized drugs are much less soluble than ionized drugs
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41
Q

Allergic reaction with ester type local anesthetics (procaine, benzocaine, tetracaine) most often is d/t ______

A

hypersensitivity to para-aminobenzoic acid (PABA)

metabolite of ester LA

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42
Q

Metformin MOA

A

Decrease hepatic gluconeogenesis and increase insulin sensitivity

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43
Q

Metformin is excreted by the ____.

Common adverse effect to monitor for?

A

kidneys

- if kidney disease, it can build up / have poor elimination -> lactic acidosis

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44
Q

Usually metformin is continued thru the periop period. When would you make an exception and d/c the metformin?

A

If pt has renal dysfunction

- d/c metformin 24-48hrs prior to surgery

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45
Q

Why is methylene blue (1mg/kg) used for methemoglobinemia?

A

methylene blue is an antioxidant for the reduction of methemoglobin using NADPH produced from the hexose phosphate pathway

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46
Q

What is the tx choice for methemoglobinemia in pts with G6PD deficiency?

A 
Ascorbic acid (vitamin C)
- an antioxidant (electron donor), is able to reduce Fe3+ to Fe2+

*avoid methylene blue bc the hexose phosphate pathway is dysfunctional and free radicals can develop -> RBC lysis

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47
Q

Which meds can cause a transient decrease in SpO2 lasting anywhere form 30 seconds - 20 min?

A
  1. Methylene blue
  2. Indocyanine green
  3. Indigo carmine

*absorbance is lower at 630 nm, which correlates to SpO2 of 84-86% in pulse ox

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48
Q

Meds known to induce methemoglobinemia (7)

A
  1. Prilocaine
  2. Nitroglycerine
  3. Sodium nitroprusside
  4. Phenytoin
  5. Sulfonamides
  6. Metoclopramide
  7. Benzocaine
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49
Q

Clinical sx of acetaminophen overdose

A

Nonspecific

  • N/V
  • Malaise
  • abdominal pain
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50
Q

Why is N-acetylcysteine (NAC) used for acetaminophen overdose?

A

NAC provides cysteine for replenishment and maintenance of hepatic glutathione stores ->
enhances elimination pathway

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51
Q

Exogenous corticosteroids stimulate the negative feedback loop and suppress both _______

A

Corticotropin releasing hormones (CRH) and arginine vasopressin (AVP) production

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52
Q

V1 receptors
vs
V2 receptors

Where are they located?
What happens if receptors are activated?

A

V1:

  • located in vascular smooth muscle
  • ca2+ release and vasoconstriction

V2:

  • located in- the distal renal tubules and collecting ducts
  • increase water reabsorption in states of hyperosmolarity or hypovolemia
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53
Q

How do loop diuretics cause a constriction alkalosis?

A

Loop diuretics inhibit the Na/K/2Cl channel in the LOH

  • Increase urine output
  • Urine is high sodium, low bicarbonate containing fluid
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54
Q

What metabolic derangements are associated w/ aspirin overdose?

A

Initially: respiratory alkalosis

Eventually: metabolic acidosis

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55
Q

Which organs are at increased risk of injury from propofol infusion syndrome (PRIS)?

A
  1. Cardiac muscle
    - HF
  2. Skeletal muscle
    - Rhabdo
  3. Liver
  4. Pancreas
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56
Q

Why do some pts have green urine with propofol infusion syndrome (PRIS)?

A

Phenol excretion

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57
Q

Why is methadone a good choice for pts with chronic neuropathic pain?

A

It is an opioid analgesic with concurrent NMDA antagonistic properties

Also provides serotonin reuptake

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58
Q

How does nitrous oxide affect pts with B12 deficiency?

What symptoms can get exacerbated?

A

Reacts with and inactivates B12 -> worsening B12 deficiency

Megalobastic anemia
Myelopathy
Neuropathy
Encephalopathy

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59
Q

Name the toxic inhalational reaction:
Nitrous oxide:
Methoxyflurane:
Halothane:

A

Nitrous oxide: B12 deficiency
Methoxyflurane: polyuric renal insufficiency
Halothane: subclinical or fulminant hepatotoxicity

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60
Q

Max dose of bupivacaine

With and without epi

A

Without epi: 2.5 mg/kg

With epi: 2.5 mg/kg

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61
Q

Max dose of chloroprocaine

With and without epi

A

Without epi: 11 mg/kg

With epi: 14 mg/kg

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62
Q

1% drug = __mg/mL

2% drug = ___ mg/mL

A

10mg/mL

20mg/mL

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63
Q

Agents with a LOWER blood: gas partition coefficient will have a (faster/slower) onset and offset

A

FASTER

  • agent in the alveoli is also in the brain
  • hangs around longer
64
Q

Agents with a HIGHER blood: gas partition coefficient will have a (faster/slower) onset and offset

A

SLOWER

65
Q

A blood:gas partition coefficient of 10 means what?

A

[ ] of inhaled anesthetic is 10 in the blood, and 1 in the alveolar gas
- high = slower onset and offset, slower induction and emergence

66
Q

Why is epi first line tx in IgE mediated anaphylaxis?

A

stimulates alpha and beta receptors -> increasing SVR, CO, and bronchodilation

Mast cell stabilizer -> reduces systemic histamine and thromboxane levels

67
Q

When should you NOT redose the same anti-emetic?

A

if the first dose was < 6 hours prior

68
Q

ASA MOA

A

potent COX inhibitor
- prevent COX enzyme needed for production of prostaglandins (thromboxane A2, critical for platelet activation and thrombus formation)

69
Q

Does ASA cause irreversible inhibition of COX?

A

Yes

- return of normal platelet occurs in 2-5 days

70
Q

Glycopyrrolate causes (miosis/mydriasis)

A

Mydriasis
- pupillary dilation

  • Anticholinergic drug
  • competitive antagonist of ACh
71
Q

Cholinergic symptoms

- ie: acetylcholinesterase inhibitors, organophosphate poisoning (repeated receptor stimulation), nerve agents

A

SLUDGE-Mi “me”

Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis
Miosis
72
Q

Antimuscarinic drugs used in anesthesia:

A

atropine
glycopyrrolate
scopolamine

73
Q

How does neostigmine affect a phase I block (std induction of sux)?

A

Augments it

- Increases the ED95

74
Q

How does neostigmine affect a phase II block of sux?

A

Antagonizes it

*but unpredictable

75
Q

The majority of anesthetic drugs/inhaled agents DECREASES lower esophageal sphincter tone.

Which ones don’t (increases)?

A 
Succinylcholine
Acetylcholinesterase inhibitors
Antacids
Some antiemetics
- metoclopramide
76
Q

Why is metoclopramide relatively contraindicated in pts with Parkinson’s disease?

A

D2-receptor antagonism

- Worsen disease

77
Q

Why does carbamazepine SHORTEN the effects of vecuronium?

A

It is metabolized by Cyt P450, and INDUCES P450 system

- Vec is metabolized by P450

78
Q

Drugs that SHORTEN the effects of Non-depolarizing blockade

A
  1. Anticonvulsants
    - phenytoin
    - Carbamazepine
  2. Cholinesterase inhibitors
    - neostigmine
79
Q

Drugs that PROLONG the effects of Non-depolarizing blockade

A

A lot (better to memorize the ones that shorten effects)

  1. Abx
  2. Antiarrhythmics
  3. Dantrolene
  4. Ketamine
  5. Local anesthetics
  6. Lithium
  7. Magnesium
  8. Volatile anesthetic agents
  9. Hypocalcemia
  10. Hypermagnesemia
80
Q

Desflurane has a low blood gas partition coefficient of ____. Meaning ____

A
  1. 42
    - very little dissolved in tissues
    - Quick onset and termination of effects
81
Q

How does Hypermagnesemia and lithium PROLONG the effects of Non-depolarizing blockade

A

Blocks calcium from entering alpha motor neurons -> preventing release of some ACh containing vesicles

82
Q

What type of antiarrhythmic can exacerbate bronchospasm in pts with asthma?

A

Nonspecific (beta1 and beta2) beta-blockade

83
Q

What are Morphine’s active and inactive metabolites?

A

Active: Morphine-6-glucuronide

Inactive: Morphine-3-glucuronide

84
Q

What happens if morphine’s active metabolite, M-6-G builds up?

A

Highly potent

- significant respiratory depression in renal failure d/t accumulation from delayed excretion

85
Q

What happens if morphine’s inactive metabolite, M-3-G builds up?

A

Neuroexcitatory effects

  • myoclonus
  • allodynia
  • seizures
86
Q

What happens to barbiturates in the setting of renal and/or hepatic failure?

A

Decreased protein binding

- increased sensitivity d/t higher concentrations of free active molecules

87
Q

How is mivacurium cleared?

A

hydrolyzed by pseudocholinesterase

*very similar to succinylcholine

88
Q

Meperidine molecule resembles what drug? What side effect is expected?

A

Atropine

- tachycardia

89
Q

Diphenhydramine MOA

A
  1. Antihistamine
  2. Anticholinergic
  3. SNRI
  4. potentiates opioid induced analgesia
90
Q

Chronic Dantrolene use is associated with ______.

A

Liver failure

- check LFT

91
Q

Why does barium hydroxide absorbents produce more carbon monoxide than soda lime?

A

D/t decreased water content of hydroxide absorbents

92
Q

What does ketamine increase?

A 
CBF
ICP
CMRO2
IOP
Salivation
Lacrimation
HR
BP
93
Q

Why shouldn’t you give pts on digoxin Calcium if their K is severely high?
(Dig can cause hyperK)

A

Digoxin inhibits Na-K ATPase -> inc intracellular Ca2+ to improve inotropy
- if you give more Ca2+ -> lethal “stone heart”

94
Q

Anaphylaxis is a type _____ hypersensitivity reaction

A

Type 1

  • Antigens bind to IgE antibodies on mast cells and basophils
  • If activated -> Hypotension, bronchospasm, urticaria

*NMBs most common offenders

95
Q

What lab should you check in pts with suspected anaphylaxis?

A

Tryptase

  • released from mast cells when activated by IgE
  • half life is 2 hours
96
Q

What are the causes of anaphylaxis in Amino ester LAs vs Amino amide LAs?

A

Esters: PABA

Amides: Methylparaben preservative (structurally similar to PABA)

97
Q

Metabolic derrangements associated with Thiazide diuretics

A

HYPO

  • Hypokalemia
  • Hypomagnesemia
  • Hyponatremia

HYPER

  • Hypercalcemia
  • Hyperuricemia
  • Hyperglycemia
  • Hypercholesterolemia
  • Hypertriglyceridemia
98
Q

Local anesthetics with lower pKa to physiologic pH will have more drug in which form?

A

Nonionized
- more drug available for use

*exception is 2-chloroprocaine with pKa of 9, works faster than bupi with pKa of 8, but that is d/t [ ] effect

99
Q

Btwn desflurane, sevoflurane, isoflurane, which is the most lipid soluble? What is this d/t?

A

Isoflurane: 91
- lipid solubility aka oil:gas partition coefficient

*Sevo is 47
Des is 19

100
Q

Which one is correlated to the SPEED of onset and offset of an anesthetic, blood-gas partition coefficient or the oil:gas partition coefficient?

A

blood-gas partition coefficient
Isoflurane&raquo_space; sevoflurane > desflurane
inversely proportional to speed of onset and offset
Desflurane > sevoflurane&raquo_space; isoflurane

101
Q

Which one is correlated to the POTENCY of an anesthetic, blood-gas partition coefficient or the oil:gas partition coefficient?

A

lipid solubility aka oil:gas partition coefficient

Isoflurane (MAC 1) > sevoflurane (MAC 2)&raquo_space; desflurane (MAC 6)&raquo_space;> nitrous oxide (MAC 104)

102
Q

Milrinone MOA

A

PDE III inhibitor,
- inc intracellular cAMP lvls -> inc calcium stores -> inc cardiac inotropy and peripheral and pulmonary vasodilation

*inodilator = Inotropy + vasodilation

103
Q

The order of volatile anesthetic potentiation of NDNMBs?

A

Desflurane > sevo > iso > halothane > TIVA

104
Q

All V/Q mismatch has which 2 effects on alveolar and arterial partial pressure?

A
  1. INCREASES alveolar anesthetic partial pressure
  2. DECREASES arterial anesthetic partial pressure

*degree of change is dependent on the solubility of the inhalational agent

105
Q

When perfusion is decreased (ie. reduced cardiac output, pulmonary embolism), what happens to the speed of induction of inhalational agent?

A

INCREASED

  • more so with soluble agents like isoflurane:
  • lipid solubility aka oil:gas partition coefficient of 91
  • The rise of FA/FI is steeper with lower perfusion of the lungs
106
Q

When ventilation is decreased (ie. intrapulmonary shunt), what happens to the speed of induction of inhalational agent?

A

DECREASED

  • more so with insoluble agents (desflurane)
  • lipid solubility aka oil:gas partition coefficient of 19
107
Q

What is the efficacy of a drug?

A

The maximum effect produced by the drug, does not depend on dose
- potency is not related to maximal effect at all

108
Q

What is the potency of a drug?

A

POTENCY is the Relative dose required to achieve given effect (related to receptor affinity)

  • EFFICACY is the opposite and has nothing to do with dose
109
Q

The difference between morphine and buprenorphine is based on (efficacy / potency)

A

efficacy (max effect of drug)

  • morphine is full agonist
  • buprenorphine is partial agonist
110
Q

The difference between isoflurane and desflurane is based on (efficacy / potency)

A

potency (dose required to produce given effect)

111
Q

Dextromethorphane MOA

A

Over the counter cough suppressant with NMDA antagonist properties
- high doses = dissociative anesthetic

112
Q

Drugs that have NMDA receptor antagonist properties

A 
Ketamine
Magnesium
Nitrous oxide
Methadone
Tramadol
Dextromethorphan
113
Q

Most common problem with dobutamine?

A

tachyarrhythmias

114
Q

Drug of choice to increase heart rate in a denervated heart

A

Isoproterenol
- beta agonist

*denervated heart cannot respond to antimuscarinic meds, needs direct agonism

115
Q

Supplements assoc with inc risk of bleeding

A

Vit E
GInger
Ginko
Garlic

116
Q

What is Ma-huang herbal supplement used for and what adverse effects are assoc?

A

weight loss

  • herbal supplement of Ephedra plant
  • HTN, Palpitations, CVA, sz
117
Q

Which drug can cause dose dependent inhibition of adrenal mitochondrial 11-B-hydroxylase?

A

Etomidate

- can cause adrenal cortisol suppression

118
Q

Do you worry about nicardipine in renal failure or hepatic insufficiency?

A

Hepatic insufficiency

- prolonged half life

119
Q

MOA of nicardipine

A

CCB

  • coronary and peripheral arterial dilator
  • antihypertensive in neurosurgical pts
  • does NOT decrease cardiac fxn
  • increases HR d/t sympathetic activation NOT baroreceptor response
120
Q

What dose of magnesium do we expect to see QRS prolongation?

A

6-12 mg/dL
- goal in obstetrics are 4.8-9.6

*nl levels are 1.8-2.5 mg/dL

121
Q

Magnesium effects on NDMBs?

A

increases sensitivity

  • need to decrease dose
  • presynaptic CCB (prevents calcium release into synaptic cleft) -> less ACh to compete
122
Q

Tx for hypermagnesemia (muscle weakness, respiratory depression, hypotension, bradycardia, prolong QRS)

A

IV calcium

123
Q

Echothiophate MOA

A

anticholinesterase used to tx refractory glaucoma by causing miosis
- can potentiate succinylcholine. May take 4-6 weeks after d/c to return to nl

124
Q

Does bumex, spironolactone and amiloride cause hyperkalemia?

A

bumex
- no, its used to tx hyperK

Spironolactone and Amiloride
- yes, blocks aldosterone -> hyperK

125
Q

Do ACEi and ARBs cause hyperK or hypoK?

A

Hyperkalemia
- inhibit angiotensin II -> prevents aldosterone formation

*aldosterone acts on distal tubules and collecting ducts to increase Na/fluid retention and Inc K+ excretion

126
Q

Concern regarding St. Johns wort (antidepressant)?

A

Cyt P450 inducer

- results in subtherapeutic drug levels, inc risk of transplant rejection (on cyclosporine), DVT (on warfarin)

127
Q

Mivacurium is a NMB

- effects in pts with pseudocholinesterase / butyrylcholinesterase deficiency?

A

DOA is prolonged in pts with deficiency

- It is metabolized by pseudocholinesterase / plasma cholinesterase / butyrylcholinesterase

128
Q

What are the most common variants in pts with pseudocholinesterase / butyrylcholinesterase deficiency

A

A and K variants

129
Q

Succinylcholine is a NMB

- effects in pts with pseudocholinesterase / butyrylcholinesterase deficiency?

A

DOA is prolonged in pts with deficiency

130
Q

Lorazepam and Oxazepam metabolism

A

Glucuronidation w/o any phase I metabolism

- less affected by age and renal disease

131
Q

All Benzodiazepines undergo metabolism where?

A

in Liver either by:
- Phase I metabolism (N-dealkylation or aliphatic hydroxylation)
or
- Phase II metabolism (glucuronidation or acetylation)

132
Q

Midazolam and Diazepam metabolism

A

Hepatic oxidation-reduction

- clearance decreases with age

133
Q

Barbiturates are (inducers/inhibitors) of cyt P450, drugs that undergo elimination via that system will require what sort of drug dosage adjustment?

A

INDUCERS
increases in drug doses

  • note: phenytoin, rifampin, carbamazepine, ethanol are all P450 inducers
134
Q

How is propofol metabolized?

A

Hepatic glucuronidation

135
Q

How are ester local anesthetics metabolized?

A

Pseudocholinesterase

136
Q

how is clonidine (alpha 2) helpful in post op period?

A

Pain control
Reduce post op shivering
Reduce PONV

137
Q

How can you differentiate anaphylactic rxn vs anaphylactoid rxn?

A

You cannot
- both histamine mediated

Anaphylaxis: IgE mediated mast cell degranulation and histamine release
Anaphylactoid: uncontrolled histamine release not involving IgE
- Mast cell tryptase levels rise in both

138
Q

Use of opioids as adjuncts for neuraxial anesthesia enhances block quality, density, and duration.
- What side effects are greatly increased?

A
  1. sedation
  2. Respiratory depression
  3. Pruritus
  4. N/V**
    - Morphine (hydrophilic) > Fentanyl (lipophilic)
139
Q

Dosing for sugammadex for 2 twitches? No twitches + 1-2 post-tetanic count? Immediate reversal after 1.2 mg/kg of roc?

A

2 twitches: 2 mg/kg
No twitches + 1-2 post-tetanic count: 4mg/kg
Immediate reversal after 1.2 mg/kg of roc: 16mg/kg

140
Q

MOA and DOA of naloxone?

A

Opioid antagonist (competes for mu, kappa, sigma receptor)

30-60 min

  • renarcotization
  • better for rev. short acting opioids
141
Q

Pts most at risk of emergence rxn receiving lg doses ketamine?

A

Older female with psych hx

142
Q

Ketamine effect on ICP? CMRO2

A

Increases both

- avoid in head injury or intracranial mass lesions

143
Q

Why is EMLA cream avoided in pts with methemoglobinemia or G6PD deficiency?

A

its a mixture of LA, likely d/t the prilocaine in the formula
- oxidizes hemoglobin to methemoglobin

144
Q

Contraindications to EMLA

A
  1. Allergy to amide anesthetics
  2. Concomitant class II anti-arrhythmics
  3. COngenital or idiopathic methemoglobinemia
  4. Infants < 12 mo getting tx w/ methemoglobin inducing agents
145
Q

Where is nitric oxide produced?

A

Endothelial cells

  • vasodilatory
  • anti-aggregating fx on plts

Immune cells

  • Cellular signaling and homeostasis
  • Immunomodulation

bone marrow
- mod pain response

Pancreas
- stim insulin release in pancreas

*localized effects of nitric oxide at site of production determines its function

146
Q

What is the clinical importance of volatile anesthetic metabolism?

A

It’s relation to fluoride-induced nephrotoxicity
Sevo (5%) > Iso (0.2%) > Des (<0.2%)

Sevo undergoes the most metabolism -> highest elevation in fluoride (behind methoxyfluorane)

147
Q

Dopamine receptor (agonists / antagonists) can lead to EPS

A

antagonists

- can prevent nausea

148
Q

Should you be cautious prescribing meperidine in pts with Kidney or Liver failure?

A

Both

  • metabolized in liver
  • eliminated by both

*CNS stimulant: tremors, twitches, sz

149
Q

What is the partition coefficient of fentanyl vs morphine?

A

Fentanyl: 816
- faster onset
Morphine: 1.4

*alfentanil is exception - 4x faster than fent, but d/t its lower pKA 6.5

150
Q

Nicardipine causes _____ dilation, while nitroglycerin causes _____ dilation.

A

Arteriolar
- spares preload

Venous

151
Q

Nesiratide and Sodium nitroprusside causes _______ vasodilation

A

Arteriolar AND venous

- decreases BOTH afterload and preload

152
Q

___________ is a recombinant form of BNP and causes ______

A

Nesiritide

vasodilation, natriuresis, and diuresis

153
Q

What drugs are metabolized by the CYP450 3A4 enzyme?

A
  1. alfentanil
  2. midazolam
  3. lidocaine
  4. OCPs

(think of the pain meds, OCP could also be anti-pain for pts with PCOS . . .)

ST JOHN’S WORT induces 34A, so these drugs bcomes less efficacious

154
Q

What drugs are metabolized by the CYP450 2C19 enzyme?

A
  1. Clopidogrel
  2. Prasugrel
  3. PPIs
  4. Antidepressants
155
Q

What does metoclopramide and succinylcholine have in common?

A

Both INCREASES lower esophageal sphincter tone

Anesthesia 101 (38 decks)

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